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Neurology
| Question | Answer |
|---|---|
| What are the four parts of the neurone? | dendrites, soma, axon & synapse |
| What does the dendrite do? | Receives input from other neurones and conveys signals to the soma |
| What does the soma do? | Contains the nucleus and endoplasmic reticulum - synthetic and metabolic centre |
| What does the axon do? | Conducts output signals to other neurones |
| What does the synapse do? | Output - point of communication between neurones |
| Where are unipolar neurones found? | PNS |
| Where are psuedounipolar neurones found? | Sensory system |
| Where are bipolar neurones found? | Retina |
| Where are multipolar neurones found? | Motor neurones |
| What is the main excitatory neurotransmitter? | Gultamate |
| What is the main inhibitory neurotransmitter? | GABA - to a lesser extent, glycine |
| What happens in chemical neurotransmission? | Uptake of precurosr, synthesis of transmitter, storage of transmitter, depolarisation by action potential, calcium influx through voltage activated calcium channels, calcium induced release of neurotransmitter (exocytosis), receptor activation |
| What does the ion Na+ do? | Moves into the cell causing depolarisation |
| What does the ion C2+ do? | Moves into the cell causing depolarisation |
| What does the ion Cl- do? | Moves into the cell causing hyperpolarisation |
| What does the ion K+ do? | Moves out of the cell causing hyperpolarisation |
| What is the main function of the frontal lobe? | Contains the primary motor cortex - movement |
| What is the main function of the parietal lobe? | Contains the somatosensory cortex - sensation |
| What is the main function of the occipital lobe? | Contains the visual cortex - vision |
| What is the main function of the temporal lobe? | Contains the auditory cortex - hearing |
| What cell produces myelin in the PNS? | Schwann cells |
| What are the four glial cells? | Astrocytes, oligodendrocytes, microglia & ependymal cells |
| What is the function of astrocytes? | Role in support, maintain the blood brain barrier, environmental homeostasis |
| What is the function of oligodendrocytes? | Produce myeline in the CNS |
| What is the function of microglia? | Phagocytic role - macrophages, antigen presenting cells |
| What is the function of ependymal cells? | Ciliated cuboidal/columnar epithelium that line ventricles |
| What order is the grey/white matter in, in the brain? | Grey matter outside - white matter on inside |
| What does grey matter contain? | neurones |
| What does white matter contain? | Axons |
| What are the layers of the meninges? | Dura mater, arachnoid mater & pia mater |
| What is the dura mater? | Outer tough layer of connective tissue |
| What is the arachnoid mater? | Relatively thin layer that is usually stuck to the dura |
| What is the pia mater? | Very thin layer that is attached to the surface of the brain |
| Where is CSF produced? | Choroid plexus in all 4 ventricles |
| Where is CSF reabsorbed? | Into dural venous sinuses via arachnoid granulations |
| What is the function of CSF? | Cushions the brain - internal and external force |
| What is increased CSF volume called? | Hydrocephalus |
| What arteries make up the circle of Willis? | Anterior cerebral artery, anterior communicating artery, internal carotid artery, posterior cerebral artery & posterior communicating artery |
| What are the two separating dural structures? | Falx cerebri - sickle shape between cerebral hemispheres Tentorium cerebelli - between cerebellum and cerebral hemispheres |
| What is the flow of CSF through the brain? | Later ventricles -> intraventricular foramen (Munro) -> third ventricle -> cerebral aqueduct -> fourth ventricle -> central canal (spinal cord) |
| What are the structures that make up the brain stem? | Medulla oblongata ((continuous with the spinal cord), pons, midbrain Ascending and descending tracts pass through it. Contains centres for control of: respiration, consciousness and cardiovascular |
| Where are the two enlargements of the spinal cord? | Cervical - very long roots, related to the upper limb Lumbar - very short roots, related to the lower limb |
| What information does the spinothalamic tract contain? | 2P's and 2 T's - pain, pressure, temperature & (coarse) touch |
| At what level does the spinothalamic tract cross at? | Cross at the spinal level they enter at |
| What information does the dorsal columns contain? | Fine touch, proprioception & vibration sense |
| At what level do the dorsal columns cross at? | Cross at the medulla |
| What information does the corticospinal tract contain? | Controls activity of the motor neurones in the spinal cord which innervate the trunk and limb muscles |
| At what level does the spinal cord terminate at? | L1/L2 |
| What is the structure that anchors the spinal cord | Filum terminale |
| How many pairs of spinal nerves are there? | 31 |
| What information does the rubrospinal tract contain? | Excitatory control of tone of limb flexor muscles |
| What information does the tectospinal tract contain? | Input mostly to the cervical segments |
| What information does the vestibulospinal tract contain? | Excitatory input to "anti-gravity" muscles |
| What are the headache red flags? | -New onset headache in a patient above 55 -Known/previous malignancy -Immunosuppressed -Early morning headache -Exacerbation by valsalva |
| Tight band sensation, pressure behind the eyes, throbbing and bursting sensations? | Tension headache |
| What are the signs of tension headache? | Tenderness and tension in the neck and scalp muscles |
| What are the features of a pressure (intra-cranial lesion) headache? | - Intracranial mass lesions - pain provoked by displaced/stretched meninges and vessels or by changes in CSF pressure (e.g. coughing, sneezing) - Typically worse on lying down - Worse in the morning - Often accompanied by vomiting |
| What is the defining feature of a low CSF volume headache? | Seen typically on standing up |
| Pain over inflamed temporal/occipital arteries, jaw claudication, pain in the face | Temporal arteritis |
| How would you diagnose and treat temporal arteritis? | Vessel biopsy and high dose prednisolone |
| Neck stiffness, vomiting and a rash ± fever? | Bacterial meningitis |
| What is a migraine? | Recurrent headache with visual and gastrointestinal disturbance |
| What factors may precipitate migraines? | Weekend, chocolate, cheese, noise and irritating lights |
| What ages and sex is migraine commonly found in? | Common around puberty and at the menopause - sometimes increases in severity or frequency with hormonal contraceptives, in pregnancy, the onset of hypertension or following minor head trauma |
| What auras are common in migraine? | Unilateral patchy scotoma, hemianopic symptoms, teichopsia (flashes) and fortification spectra (jagged lines) |
| How long does the aura part of a migraine with aura last, and how long does he consequent headache last? | Aura - 20-60 minutes, Headache <1 hour |
| What features are needed for a diagnosis of migraine without aura? | - Prodromal visual symptoms are vague - At least 5 attacks - 4-72 hour duration |
| What investigations are typically needed for a suspected migraine? | None |
| What may trigger a migraine with aura? | Sleep, diet, stress, hormones and physical exertion |
| What is the acute management of a migraine? | paracetamol/NSAIDs (ibuprofen, neproxen, diclofenac) - ± anti-emetic (metaclopramide) triptans - rizatriptan/eletriptan - more expensive so start with NSAID |
| What is the prophylactic management of a migraine? | Propranolol (beta blocker)- avoid in asthma, PVD and heart failure Topiramate (carbonic anhydrase inhibitor) - poor side effect profile (memory impairment) Amitriptyline (TCA) - dry mouth |
| Cluster headache? | Recurrent bouts of excruciating sudden onset unilateral retro-orbital pain lasting 30-90 minutes with parasympathetic innervation in the same eye (ptosis, miosis, congestion & tearing) |
| Epidemiology of cluster headache? | 30-40s, M>F |
| Headache pain "worse than childbirth"? | Cluster headache |
| Treatment of cluster headache? | High flow oxygen for 20 minutes, subcutaneous sumatriptan, steroids, verapamil for prophylaxis Analgesics are unhelpful |
| Trigeminal neuralgia? | Severe stabbing unilateral pain lasting 1-90 seconds, can gave 10-100 attacks a day |
| Treatment of trigeminal neuralgia? | Cabamazepine, gabapentin, phenytoin, baclofen - Surgery: ablation vs decompression |
| Types of gait disorders? | Spastic, extrapyramidal (Parkinson's), apraxic, ataxic, myopathic, psychogenic, antalgic |
| Spastic gait? | Stiff, jerky circumduction of legs ± scuffing feet - May be seen in tumour, abscess, cerebral palsy and multiple sclerosis |
| Antalgic gait? | Gait develops to avoid pain Trauma, osteoarthritis etc |
| Extrapyramidal gait? | Flexed posture, shuffling feet, slow to start, postural instability, stoop, difficulty turning, retropulsion Parkinson's |
| Cerebellar ataxic gait? | Broad based gait, veer to side of affected lobe when walking Causes - focal lesions, B12, hypothyroidism, Wilson's |
| Sensory ataxic gait? | Loss of proprioception, broad based, high stepping, stamping gait develops - Positive Romberg's test - Cause: polyneuropathy |
| Myopathic gait? | Foot drop - common fibular palsy - foot hits ground with audible slap Weakness of proximal lower limb muscles - polymyositis, muscular dystrophy - walking becomes waddled |
| Apraxic gait? | Frontal lobe disease - acquired walking skills become disorganised - 'gluing to the floor''novice on ice' |
| Pyschogenic gait? | Bizarre gait, not conforming to any organic disorder - common with anxiety and depression |
| Types of movement disorder? | Myoclonus, tremor, dystonia, chorea and tics |
| "Pill rolling" tremor? | Parkinson's |
| Chorea? | Jerky, quasi, puposive, explosive fidgety movements, flitting around the body |
| Sydenham's chorea? | - Transient post-infective chorea in children and young adults - About half of cases follow rheumatic fever - Onset is gradual - Recovery occurs spontaneously within weeks or months |
| Causes of chorea? | Huntington's, Sydenham's, drugs (phenytoin, levodopa, alcohol), thyrotoxicosis, pregnancy and OCP, hypoparathyroidism, SLE, stroke |
| Myoclonus? | Sudden, involuntary jerking of a single muscle or group of muscles |
| Dystonia? | Movement caused by prolonged muscular contraction - part of the body is thrown into spasm |
| Treatment of dystonias? | Botox injections, sometimes antimuscarinics |
| Tics? | Common, brief stereotyped movements, usually affecting the face/neck but may affect any body part, including vocal tics |
| Spasmodic torticollis? | Dystonic spasms gradually developing around the neck, cause the head to turn or to be drawn backwards or forwards |
| What is Huntington's disease? | Relentlessly progressive chorea and dementia Autosomal dominant, mutation of chromosome 4 |
| What is the pathology of Huntington's? | Cerebral atrophy progresses, marked loss of neurones - Changes in neurotransmitters |
| Symptoms of Huntington's? | Triad - emotional, cognitive and motor disturbance - Depression, irritability and apathy - Dementia - Chorea, myoclonus, involuntary movements, dysphagia |
| What is the prognosis of Huntington's? | Death within 15 years of diagnosis |
| Treatment of Huntington's? | Sulpiride and tetrabenazine (both forms of dopamine blockers) - help chorea |
| What is multiple sclerosis? | Chronic inflammatory disorder - multiple plaques of demyelination within the brain and spinal cord (CNS only) - T cell mediated immune response - plaques are disseminated in both time and place |
| Symptoms of multiple sclerosis? | - Motor weakness - Optic neuritis - painful loss of vision - Pain, paraesthesiae, loss of proprioception & vibration (dorsal column loss) - Cognitive impairment - Fatigue - Lower urinary tract dysfunction - frequency, urgency etc - Ataxia, tremor, n |
| Investigation of MS? | MRI of brain and cord is the definitive structural investigation - CSF: oligoclonal IgG bands |
| Symptomatic treatment of MS? | - Mild: physio/OT, treat fatigue (amantadine), treat spasticity (baclofenac, IM botox), treat sensory (gabapentin, amitriptyline), urinary (oxybutynin, desmopressin) - Moderate: oral steroids (methylprednisolone) - Severe: admit and IV steroids |
| Preventing relapse and disability of MS? | Beta-interferon - avonex, betaseron, extavia |
| Disease modifying therapy in MS? | 1st line - interferon beta (avonex, betaseron, extavia), copaxon (slow onset), tecfidera 2nd line - tysabri (associated with PML), fingolimid 3rd line - mitoxantone - cardiac toxicity dose related |
| What is progressive multifocal leukoencephalopathy? | - Rapidly progressive, demyelinating, CNS disease caused by the opportunistic pathogen JC virus - Occurs in the immunocompromised only |
| Symptoms of PML? | Clumsiness, progressive weakness, visual, speech and sometimes personality change |
| Treatment of PML? | Reversing immune deficiency - in HIV give HAART |
| What is epilepsy? | a recurrent tendency to have spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting as a seizure |
| What is epilepsies EEG hallmark? | High voltage spike and wave activity |
| What are the two broad classifications of epilepsy? | Focal and generalised |
| What are the types of generalised epilepsy? | Absence, tonic clonic, myoclonic, tonic, clonic, atonic |
| Very brief seizure, activtity ceases and the patient stares and pales slightly for a few seconds, twitching of eyelids, start of childhood? | Absence seizures - petit mal |
| What do children with absence seizures tend to develop in adult life? | generalised tonic clonic seizures |
| What is a tonic clonic seizure? | Vague warning -> tonic phase, body becomes rigid for up to a minute -> patient utters a cry and falls -> clonic phase, generalised convulsions, frothing at the mouth, bilateral rhythmic jerking of the muscles, seconds to minutes -> drowsiness/confusion |
| What is a myoclonic seizure? | Isolated muscle jerking |
| What is a partial (focal) seizure? | Electrical abnormality is localised to one part of the brain - underlying structural cause - most common in elderly |
| What is the defining feature between types of partial seizure? | Loss of awareness - in simple there is no loss of awareness - in complex there is loss of awareness |
| What is a seizure? | Unresponsive, rigid body (extended arms and legs, head turned), jerking of limbs, look red, eyes open, disorientated after return of consciousness |
| What can cause seizures? | Encephalitis, cerebral abscess, tuberculoma, cortical venous thrombosis and neurosyphilis, chronic meningitis (TB), acute bacterial meningitis, chronic alcohol abuse, withdrawal of antiepileptic drugs and benzodiazepines, metabolic disturbances |
| What is crucial in history taking in suspected epilepsy? | Involvement of a witness |
| What would you ask about in a epilepsy consultation? | Onset - what they were doing and where? How did they look? How did they feel?| Event itself - type of movements, responsiveness, awareness?| Afterwards = speed of recovery?| PMH| DH |
| What is syncope? | Sweaty, light headed, pale, loss of consciousness, quick recovery |
| How would you examine a patient in suspected syncope? | Cardiovascular examination and lying+standing BP |
| What is status epilepticus? | Medical emergency, continuous seizures without recovery of consciousness, lasts over 30 minutes |
| How would you treat status epilepticus? | Lorazepam and phenytoin |
| What is the treatment of generalised epilepsy? | Sodium valproate, although teratogenic so may give females lamotrigine |
| What is the treatment of focal epilepsy? | Carbamazepine or lamotrigine |
| What are the adverse effects of sodium valproate? | Weight gain, teratogenic, hair loss and fatigue |
| What is SUDEP? | Sudden death in epilepsy, more than doubles chances of dying young (<35). If have severe epilepsy can be as high chance as 1/100 |
| What is the birth defect risk in babies of mothers who take on AED? | Around 7%, normal population is 3% |
| How do some anti-epileptic drugs influence COPC and morning after pills? | Reduce efficacy |
| What are the driving rules for someone with epilepsy? | Have to be seizure free for 12 months to drive a motor vehicle |
| When would you suspect a functional attack? | Uncontrollable symptoms, no learning disabilities & CNS exam, CT, MRI and EEG normal |
| The patient has reduced speech fluency with relatively preserved comprehension, few disjointed words with failure to construct sentences? | Broca's expressive aphasia - infero-lateral dominant frontal lobe lesion |
| Patient has fluent language but words are muddled and often sentences are often jargon heavy, theres is loss of comprehension? | Wernicke's receptive aphasia - posterior superior dominant temporal lobe lesion |
| The patient has difficulty naming familiar objects? | Nominal aphasia - posterior dominant tempoparietal lesions |
| What is dysarthria? | Disordered articulation - due to paralysis, slowing or inco-ordination of muscles of articulation or local discomfort |
| What diseases is dysarthria seen in? | Psuedobulbar palsy: gravelly speech - Cerebellar lesions: jerky, ataxic speech - Parkinson's: monotone - Myasthenia gravis - speech that fatigues and dies away |
| What commonly causes viral meningitis? | Enteroviruses - echoviruses, coxsackei virus, mumps |
| Who is typically affected by viral meningitis? | Children |
| What are the symptoms of viral meningitis? | Headache, fever, stiff neck and photophobia |
| What is the course of viral meningitis? | Self-limiting |
| What is the treatment of viral meningitis? | Supportive |
| How is viral meningitis investigated? And what would the findings be? | Lumbar puncture - raised WCC (predominantly lymphocytes), RCC raised, protein and glucose normal |
| What are the most common causes of neonatal bacterial meningitis? And how are they treated? | Listeria: amoxicillin + gentamycin - Group B strep - benzylpenicillin + gentamicin - E. coli: cefotaxime + gentamicin |
| What is the most common cause of childhood bacterial meningitis? And what is the treatment? | H. influenzae - normal throat microbiota, requires blood factors for growth, type b is most common cause in this age group - IV ceftriaxone - vaccine now available |
| What is the most common cause of bacterial meningitis in those aged between 10-21? And what is the treatment? | Neisseria meningitis (meningococcal) found in the throats of healthy carriers- symptoms due to endotoxin - IV ceftriaxone |
| What is the most common cause of bacterial meningitis in those aged 21 and over? And what is the treatment? | Step pneumoniae (pneumococcal) - common in nasopharynx - IV ceftriaxone |
| What is the most common cause of acute meningitis in immunocompromised patients? And what is the treatment? | Listeria monocytogenes (gram positive bacilli) - IV ampicillin/ amoxicillin - ceftrixone of no value | also affects neonates and elederly |
| What are the symptoms of acute bacterial meningitis? | Headache, alteration in consciousness, neck stiffness, fever, vomiting, pyrexia, photophobia, lethargy, confusion, rash, positive Kernig's sign |
| What is Kernig's sign? | Severe stiffness of the hamstrings leading to an inability to straighten the leg when the hip is flexed to 90 degrees |
| What would you expect to find on CSF findings in bacterial meningitis? (white cells count, neutrophils, protein, glucose, glu (CSF/serum) | WBC > 2000, Neutrophils > 1,180, Protein >220mg/dl, Glucose <34 mg/dl, glu <0.23 |
| What is the pathogenesis of acute bacterial meningitis? | Nasopharyngeal colonisation, direct extension of bacteria - sinusitis, otitis, cranial trauma, blood borne infection |
| What is the management of bacterial meningitis? | Immediate IV antibiotics - ceftriaxone (if penicillin allergic -> cefotaxime), blood cultures, prophylaxis of contacts (rifampicin in kids, ciprofloxacin for adults) |
| Indications for hospital management in acute adult bacterial meningitis? | Signs of meningeal irritation, impaired conscious level, petechial rash, febrile/unwell/recent fit |
| Management on hospital admission for suspected acute adult bacterial meningitis? | ABCDE, blood culture + coagulation screen, throat swab, swab any petechial/purpuric skin lesions for M+S, urgent CT, administration of antibiotics (IV ceftriaxone add IV ampicillin/amoxicillin if listeria suspected), steroids |
| What are the warning signs of acute adult bacterial meningitis? | GCS <12 or fall in GCS >2, focal neurology, seizure before or at presentation, shock, bradycardia and hypertension, papilloedema |
| What antibiotic would you give if listeria suspected and the patient was penicillin allergic? | Co-trimaxazole alone |
| What antibiotics would you give as empirical treatment for acute adult bacterial meningitis if the patient was penicillin allergic? | Chloramphenicol + vancomycin |
| How would you treat TB meningitis? | Isoniazid + rifampicin (add pyrazinamide, ethambutol) |
| What clinical features would you find in neonatal meningitis? What investigations would you do? | Clinical features can be subtle - slightly low temperature Culture blood and CSF |
| In what circumstances would you give prophylactic antibiotics for neonatal meningitis? | Pre-term labour, prolonged rupture of membranes, found incidentally to have GBS in vagina or urine, fever in labour/ammonites, GBS infection in previous baby |
| What are the non-infective causes of meningitis? | Malignant cells, intrathecal drugs, sarcoidosis/vasculitis etc |
| What cause chronic meningitis? | Tuberculous meningitis and cryptococcal meningitis, syphilis, sarcoidosis and behcet's |
| What are the clinical features of chronic meningitis? | Vague headache, lassitude, anorexia, vomiting, drowsiness, focal signs and seizures |
| Management of chronic meningitis? | Antituberculosis drugs - rifampicin, isoniazid, pyrazinamide - avoid ethambutol due to eye complications; adjuvant prednisolone |
| Inflammation of the brain parenchyma? | Encephalitis |
| What are the common causes of encephalitis? | Virus - HSV 1 (common in UK) + 2, echovirus, coxsackie, mumps, EBV, HIV| epidemic and endemic causes - japanese, ross river fever, california, west nile etc |
| What are the clinical features of viral encephalitis? | Many are mild, in minority - high fever, headache, mood change and drowsiness over hours or days, focal signs, seizures and coma ensue |
| How would you treat suspected HSV encephalitis? | IV aciclovir, seizures are treated with anticonvulsants (phenytoin) |
| In what disease would you find antibodies against voltage gated potassium channels? | Limbic encephalitis |
| What is shingles? | Herpes zoster - reactivation of varicella zoster infection within dorsal root ganglia, the original infection having been chickenpox many years previous |
| What cranial nerves does herpes zoster commonly affect? | V - trigeminal and VII - facial |
| What is ophthalmic herpes? | Infection of V1, can lead to corneal scarring and secondary panophthalmitis |
| What is Ramsey Hunt syndrome? | Geniculate herpes of the facial nerve - auditory canal involvement - tinnitus/deafness |
| What is the treatment of shingles? | Acyclovir |
| What is post-herpatic neuralgia? | Pain in a previous shingle zone - occurs in 10% - burning, continuous pain responds poorly to analgesics - gradual recovery over 2 years |
| What is the treatment of post-herpetic neuralgia? | Amitriptyline is commonly used, intrathecal methylprednisolone is sometimes helpful |
| What is neurosyphilis? | Infection of the brain or spinal cord by the spirochete Treponema pallidum |
| What serology would you expect to find with neurosyphilis? | Positive TPHA (T. pallidum haemagluttination assay) & FTA (fluorescent treponemal antibody) |
| What symptoms could you find in neurosyphilis? | Abnormal gait, blindness, confusion, dementia, depression, headache, incontinence, neuropathy, psychosis, seizures, tremors, visual disturbances, muscle weakness |
| What occurs in meningovascular syphilis? | Subacute meningitis with cranial nerve palsies and papilloedema (decreased vision), a gumma (chronic expanding intracranial mass), parapesis (a spinal meningovasculitis) |
| What features would you find in tabes dorsalis? | Demyelination in dorsal roots| Lightning pains, ataxia, stamping gait, reflex/sensory loss, wasting, neuropathic (charcot) joints, Argyll Robertson pupils (accomodates but doesn't react), ptosis and optic neuropathy |
| What is the treatment of neurosyphilis? | Benzylpenicillin in primary infection eliminates any risk of neurosyphilis in primary infection| Steroid cover with penicillin to arrest neurological disease |
| What is neurocysticercosis? | Ingestion of eggs of Taenia solium (e.g. pork tapeworm)| Main cause of acquired epilepsy, endemic in parts of developing world| Antiparasitic treatment with albendazole |
| What is Behcet's syndrome? | Small vessel systemic vasculitis - recurrent oral and/or genital ulceration, inflammatory ocular disease, neurological syndromes - brainstem and cord lesions, aseptic meningitis, encephalitis and cerebral venous thrombosis can occur |
| What bacteria typically cause brain abscess? | Streptococcus anginosus, bacteroides species and Staphlycocci |
| What are the clinical features found in brain abscess? | Headache, focal signs, epilepsy, raised intracranial pressure, fever, leucocytosis, raised ESR |
| At what rates do cerebral and cerebellar abscesses develop at? | Cerebral abscesses may be indolent - developing over weeks; cerebellar absceses tend to develop rapidly over days or hours, producing hydrocephalus |
| What would you see on CT of a brain abscess? | Thin high-attenuation rim |
| If streptococal or anaerobic infective cause of brain abscess what is the treatment? | Cefuroxime plus metronidazole |
| What is the treatment for a Staphylococcal infection? | Flucloxacillin with cefuroxamine |
| Chronic caseating intracranial granulomas? | Tuberculomas |
| What is CN I and what is its function? | Olfactory nerve - smell - not routinely tested |
| What is CN II and what is its function? | Optic nerve - vision - tested acuity, visual fields and pupillary response |
| What is CN III and what is its function? | Oculomotor - eyelid elevation, eye elevation, adduction, |
| What are the signs of a complete third nerve palsy? | Unilateral complete ptosis| eye facing down and out| fixed and dilated pupil |
| What is CN IV and what is its function? | Trochlear - superior oblique function, makes eye move down and in |
| What is CN V and what is its function? | Trigeminal - facial and corneal sensation, mastication muscles |
| What are the divisions of the trigeminal nerve? | Ophthalmic (V1), maxillary (V2) and mandibular (V3) |
| What would a complete Vth nerve lesion cause? | Unilateral sensory loss of the face, tongue and bucal mucosa, the jaw deviates to the side as the mouth opens, diminution of the corneal reflex |
| What are the features of trigeminal neuralgia? | Knife-like or electric shock pain, lasting seconds, occurring in the distribution of the Vth nerve - tends to commence in V3 and spread - spasms occur many times a day and may have stimuli |
| What is the treatment of trigeminal neuralgia? | Carbamazepine daily - if drugs fail, surgery is useful - decompresion vs ablation |
| What is CN VI and whats is its function? | Abducens - eye abduction (lateral rectus) |
| What is CN VII and what is its function? | Facial - facial movement, taste - anterior 2/3rds of tongue via chorda tympani |
| What is Bell's palsy? | Common, acute, isolated facial palsy usually due to viral infection affectin CN VII |
| What are the features of Bell's palsy? | Sudden unilateral facial weakness, sometimes loss of taste on the tongue, and hyperacusis (reduced tolerance to usual environmental sound). Pain behind the ear is common at onset. |
| What is the management of Bell's palsy? | Spontaneous recovery usually begins during second week but can take 12 months - prednisolone - valaciclovir/aciclovir if severe - tape/suture the eyelids close to protect cornea - cosmetic surgery if unsightly paralysis is residual (usually 10%) |
| What is Ramsay Hunt syndrome? | Herpes zoster (shingles) of the geniculate ganglion (CN VII) |
| What are the features of Ramsay Hunt syndrome? | Facial palsy (like Bell's) with herpetic vesicles around the auditory meatus and/or the soft palate |
| What is the management of Ramsay Hunt syndrome? | Treat as for shingles - steroids and aciclovir |
| What is CN VIII and what is its function? | Vestibulo-cochlear nerve - balance and hearing |
| What are the symptoms of a cochlear nerve lesion? And how would you test? | Deafness (conductive or sensorineural) and tinnitus - Rinne's and Weber's (512Hz tuning fork) |
| What are the main symptoms of vestibular nerve lesions? | Vertigo and loss of balance - vomiting frequently accompanies any acute vertigo |
| What is vertigo? | The definite illusion of movement of the subject or surroundings, typically rotary |
| What is nystagmus, and when might it be present? | Rhythmic oscillation of eye movement - a sign of disease in the retina, oculomotor and/or vestibular systems and their connections - either jerk or perpindicular - Hallpike's test may provoke nystagmus |
| What is vestibular neuronitis? | Acute attack of isolated vertigo with nystagmus, often with vomiting, believed to follow viral infections - can last for several days or weeks - self-limiting and rarely recurs |
| What is CN IX and what is its function? | Glossopharyngeal - sensation to the soft palate and taste to the posterior 1/3 of the tongue |
| What is CN X and what is its function? | Vagus nerve - cough, palatal and vocal cord moevements |
| What is CN XI and what is its function? | Accessory - control of trapezius and sternocleidomastoid - head turning and shoulder shrugging |
| What is CN XII and what is its function? | Hypoglossal - controls tongue movements |
| What is a dermatome? | Area of skin supplied by 1 spinal nerve - sensory |
| What is a myotome? | Skeletal muscle supplied by 1 spinal nerve - motor |
| C2 dermatome? | Back of scalp and adam's apple |
| C3 dermatome? | Back of neck and jugular notch |
| C4 dermatome? | Clavicle and shoulder tip |
| C5 dermatome? | "Badge patch" |
| C6 dermatome? | Thumb and lateral forearm |
| C7 dermatome? | Middle finger |
| C8 dermatome? | LIttle finger |
| T1 dermatome? | Medial forearm |
| T2 dermatome? | Medial arm and sternal angle |
| T 4 dermatome? | Male nipple |
| T8 dermatome? | Xiphoid process |
| T10 dermatome? | Umbilicus |
| T12 dermatome? | Pubic symphisis |
| L1 dermatome? | Groin |
| L2 dermatome? | Anterior thigh |
| L3 dermatome? | Anterior knee |
| L4 dermatome? | Medial malleolus |
| L5 dermatome? | Dorsum of foot |
| S1 dermatome? | Heel |
| S2 dermatome? | Posterior knee |
| S3 dermatome? | Buttock |
| S4 dermatome? | Perineum |
| S5 dermatome? | Peri-anal skin |
| What nerves control should abduction? | C5 (deltoid) |
| What nerves control should adduction? | C5-7 |
| What nerves control elbow flexion? | C5&6 - biceps brachii |
| What nerves control elbow extension? | C7&8 - triceps brachii |
| What nerves control elbow pronation? | C6 - pronator teres and quadratus |
| What nerves control elbow supination? | C8 - supinator |
| What nerves control wrist flexion? | C6&7 |
| What nerves control wrist extension? | C7&8 |
| What nerves control finger flexion (grip strength)? | C8 |
| What nerves control finger extension? | C7 |
| What nerves control finger adduction and abduction? | T1 - dorsal and palmar interossei |
| What nerves control hip flexion? | L1-3 - psoas major |
| What nerves control hip extension? | L5,S1 - gluteus maximus and hamstrings |
| What nerves control knee flexion? | L5, S1 - hamstrings |
| What nerves control knee extension? | L3-4 - quadriceps |
| What nerves control ankle dorsiflexion? | L4-5 - tibialis anterior |
| What nerves control plantar flexion? | S1-2 - gastrocnemius/soleus |
| What nerves control ankle inversion? | L4 - tibialis anterior and posterior |
| What nerves control ankle eversion? | L5, S1 - fibularis longus and brevis |
| What is the most common cause of intracranial tumour? | Metastases - bronchus, breast, stomach, prostate, thyroid & kidney |
| What is a glioma? | Malignant tumour of neuroepithelial origin - usually within the hemispheres - e.g. astrocytomas, oligodendorgliomas |
| What is a meningioma? | Benign tumour arising from the arachnoid membrane, can erode bone, unusual below the tentorium cerebelli |
| What is a schwannoma (neurofibroma)? | Solid benign tumour arising from Schwann cells |
| What are the clinical features of a brain tumour? | Three mechanisms. 1 - direct effect, brain is destroyed and local function is impaired, focal neurological defect, 2 - raised ICP, papilloedema, vomiting, headache & gait ataxia, 3 - by provoking generalised and/or partial seizures |
| What are the features of raised intra-cranial pressure? | Headache, vomiting and papilloedema |
| What features would be present with compression of the medulla? | Impaired consciousness, respiratory depression, bradycardia, abnormal body posture |
| What is the best imaging investigation for brain tumour? | MRI - shows >95% of intracranial tumours |
| Would you carry out a lumbar puncture in a patient with suspected brain tumour? | Contraindicated when there is any possibility of a mass lesion as withdrawing CSF may provoke immediate herniation of the cerebellar tonsils |
| What is the treatment of a suspected brain tumour? | IV or oral dexamethasone for cerebral oedema - IV mannitol to reduce oedema, decreasing ICP - Carbamazepine/lamotrigine for epilepsy (focal) - Surgery if possible and necessary - Radiotherapy - gliomas and metastases - Chemotherapy has little value |
| What features are commonly seen in idiopathic/benign intracranial hypertension? | Headaches, visual blurring and papilloedema, machinery nose in ears |
| Who is idiopathic/benign intracranial hypertension found in mostly? | Obese young women with vague menstrual irregularities |
| What complications can arise from idiopathic/benign intracranial hypertension? | Optic nerve infarction - consequent blindness when papilloedema is severe and long-standing |
| What is the management of idiopathic/benign intracranial hypertension? | Repeated lumbar puncture, acetazolamide (to decrease CSF pressure) or thiazide diuretics, prednisolone for headache and papilloemdema| weight reduction is helpful| surgical decompression is sometimes necessary (lumboperitoneal shunting) |
| What is hydrocephalus? | Excessive water (SCF) within the head| usually an obstructive cause, very rarely is overproduction |
| What are the clinical features of hydrocephalus? | Headache, cognitive impairment, vomiting, papilloedema, ataxia and bilateral pyramidal signs |
| What could cause hydrocephalus? | Infantile hydrocephalus (aqueduct stenosis), tumours, SAH, head injury or meningitis (particulalry TB), 3rd ventricle colloid cyst, choroid plexus papilloma (rare) secretes CSF |
| What is the tretment of hydrocephalus? | Ventriculo-atrial or ventriculo-peritoneal shunting| neurosurgical removal of tumours when appropriate |
| What is normal pressure hydrocephalus? | Syndrome of enlarged ventricles, dementia, urinary incontinence and gait apraxia, usually in the elderly - CSF pressure and constituents are typically normal |
| What is bulbar palsy? | Lower motor neurone weakness of muscles whose cranial nerve (IX-XII) nuclei lie in the medulla (bulb) |
| What are the clinical features of bulbar palsy? | Flaccid, fasciculating tongue (sac of worms)| absent jaw jerk (or normal)| speech is quiet, hoarse or nasal |
| What is pseudobulbar palsy? | Bilateral upper motor neurone lesions of lower cranial nerves - corticobulbar tract |
| What are the clinical features of pseudobulbar palsy? | Weakness of the tongue and pharyngeal muscles - stiff, slow spastic tongue (not wasted), dysarthria with a stiff, slow voice (dry and gravelly) and dysphagia - gag and palatal reflexes are preserved and the jaw jerk is exaggerated - emotional lability |
| What is emotional lability? | Inappropriate laughing or crying - often present in pseudo-bulbar palsy |
| What is a absence seizure? | Brief pause in activity less than 10 seconds, affects children - unresponsive to stimuli but still conscious, quick recovery, risk tonic-clonic later in life - 3Hz spike and wave pattern on EEG - generalised seizure treat with valproate |
| What is a atonic seizure? | Sudden loss of tone, flaccidity is the key word - looks like a faint, consciousness is preserved - primary generalised seizure, treat with valproate - usually begins in childhood, continues into adulthood |
| What is a tonic clonic seizure? | Tonic phase (stiff, tongue biting, legs extended, arms flexed, pupils dilated, cyanosis (not breathing)) followed by clonic (convulsions, limb jerking, frothy, eyes roll) - lose consciousness, post-ictal confusion - treat with valproate |
| What is a Jacksonian seizure? | Partial (focal) seizure affecting the frontal lobe - primary motor cortex - one side of body - progresses from twitching/tingling in a finger/big toe/corner of mouth then marches over a few seconds to the entire hand/foot/facial muscles - Carbamazepine |
| What is a temporal lobe seizure? | Partial seizure - unreality, depersonalisation, derealisation classic as is hallucinations (visual/smell/taste) - deja vu/emotional disturbance - dysphasia during/post-ictal - vomiting, diarhhoea etc - carbamazepine |
| What is a functional seizure? | Non-epileptic attack disorder - psychological cause, not consciously mediated - negative memory replayed triggers seizure - duration over 2 mins, gradual onset, fluctuating course, violent thrashing movements, side to side head movements - CBT etc |
| What is a febrile convulsion? | Usually kids aged 6 months-5 years, boys more than girls - usually associated with viral infection, no underlying CNS infection - generalised tonic-clonic seizure usually only a few mins - genetic predisposition, ^risk epilepsy, benzos if prolonged |
| What are the features of a subdural haemorrhage? | Subdural haematoma due to tearing of bridging veins in subdural space - old people have cerebral atrophy - alcohol commonly involved - gradual onset, can often be chronic in elderly - crescent shape on CT |
| What are the features of a subarachnoid haemorrhage? | Usually due to berry aneurysms, hypertension and smoking increase risk of bleed - explosive sudden onset - signs of meninginisms (vomiting, photophobia, neck pain - xanthrochromia (yellowing of CSF) |
| What is the treatment of subarachnoid haemorrhage? | Nimodipine to prevent cerebral ischaemia, nitroprusside as a vasodilator for hypertension - CT angio to treat aneurysm |
| What are the features of giant cell arteritis? | Headache, tenderness, pain in jaw muscles, vasculitis |
| What is the treatment of giant cell arteritis? | Steroids and aspirin |
| What is the treatment of benign intracranial hypertension? | Prednisolone acutely, acetazolamide chronically to reduce ICP |
| What is the treatment of cluster headaches? | Acutely - sumatriptan + high flow ozygen | Prevention - verapamil |
| What aspects of sensation would be affected in left T10 cord compression? | Ipsilateral dorsal column - fine touch, vibration and proprioception | Contralateral spinothalamic - pain and temperature| Below the umbilicus |
| What are the features of central cord syndrome? | Loss of pain and temperature (spinothalamic) sensation of both arms and upper chest, proprioception and fine touch are relatively unaffected - cape like spinothalamic loss, legs okay - usually due to hyperextension in patient with cervical spondylosis |
| WHat are the features of a conus lesion? | Most distal part of spinal cord (T12-L2) before cauda equina - more lower back pain - symmetric hyperreflexic distal paresis of lower legs - fasciculations - ED common, more sudden bilateral presentation |
| What do posterior (dorsal) roots of the spinal cord carry? | Sensory fibres towards the cord |
| What do anterior (ventral) roots of the spinal cord carry? | Motor fibres away from the cord |
| What is the function of the corticospinal tract? | Carried descending motor fibres, cross at medulla |
| What is the functional of the dorsal column? | Carriers ascending neurones mediating fine touch, vibration and proprioception, ascend on same side and cross at the medulla - symptoms on same side |
| What is the function of the spinocerebellar tract? | Ascending sensory tract, carries fibres for proprioception from lower limb |
| What is the function of the spinothalamic tract? | Ascending sensory tract, neurones responding to pain and temperature, cross at spinal level - gives symptoms on opposite side |
| What is the function of the reticulospinal tract? | Descending motor tract involved in posture and crude, imprecise movements, originate in the reticular fomation |
| What are examples of corticospinal/pyramidal/UMN symptoms? | Drift of the upper limb when outstretched| Weakness and loss of skilled movement| Changes in tone and tendon reflexes (initially flaccid then spasticity)| Changes in superficial reflexes| No muscle wasting| Normal electrical excitability of muscles |
| What will a lesion in the motor cortex cause? | Weakness and/or loss of skilled movement confined to one contralateral limb - a defect in cognitive function (e.g. aphasia) and focal epilepsy may occur |
| What will a lesion in the internal capsule cause in relation to the corticospinal tract? | Small lesion cause a large deficit as fibres are tightly packed - can get sudden, dense, contralateral hemiplegias |
| What will a lesion in the pons cause in relation to the corticospinal tract? | Rarely confined to the corrticospinal tract -adjacent structures may be involved - CN VI and VII nuclei - dipolopia, facial weakness etc |
| What will a lesion in the spinal cord cause in relation to the corticospinal tract? | |
| Why is ceftriaxone used in bacterial meningitis? | Has a longer half-life than penicillin so needs fewer doses and so is more likely to be used effectively |
| What circumstances would you see tuberculous meningitis in, and how would you treat? | Reactivation, elderly - previous TB seen on CXR - high index of suspicion - isoniazid + rifampicin key (add pyrazinamide + ethambutol) |
| What is cryptococcal meningitis and how is it treated? | Fungal, mainly seen in HIV disease - CD4 <100 - disseminated infection - subtle neurological presentation - aseptic on CSF - cryptococcal antigen present - IV amphotericin B/flucytosine - fluconazole |
| What are the principles of lumbar puncture in suspected meningitis? | LP only if clinically feasible - be cautious if increased ICP possible, do CT - treat with antibiotics first - utilise sitting position if necessary - haematology, microbiology, chemistry & second haematology bottles |
| What are the typical CSF findings in viral meningitis? | Lymphocytes - negative gram stain - negtaive bacterial antigen detection - normal or slightly high protein - glucose usually normal |
| What are the typical CSF findings in bacterial meningitis? | Predominantly polymorphs - positive for gram stain - positive bacterial antigen detection - blood glucose reduced - high protein |
| What are the typical CSF findings in tuberculous meningitis? | Predominantly lymphocytes - gram stain can be positive or negative - high or very high protein - blood glucose reduced |
| What is "aseptic" meningitis? | Term used to mean non-pyogenic bacterial meningitis - spinal fluid formula with low number of WBC, minimally elevated protein, normal glucose - can be infectious (HSV, syphilis, TB, cryptococcus etc) or non-infectious (carcinomatous, sarcoidosis etc) |
| What are the indications for hospital admission in acute adult bacterial meningitis? | Signs of meningeal irritation - impaired conscious level - a petechial rash - febrile or unwell - any illness, especially headache, any close contacts with meningococcal infection |
| What action should be taken on hospital admission in suspected acute adult bacterial meningitis? | Take blood and coagulation screen - treatment - throat swab - disrupt and swab or aspirate any petchial or purpuric skin lesions - CT scan in those with papilloedema or focal neurological signs |
| What are the warning signs in acute bacterial meningitis? | Marked depressive conscious level (GCS<12) or a fluctuating conscious level (fall in GCS >2) - focal neurology - seizure before or at presentation - shock - bradycardia and hypertension - papilloedema |
| What general measures can you take in treatment of acute CNS infections? | Elevate head of bad, increase venous return, decreasing ICP - monitor neurological status - assess pain and restlessness on a regular basis - administer analgesia, avoiding narcotics - dark, quiet room |
| When should steroids be given in suspected bacterial meningitis? | Before or with the first dose of antiobiotics and then every 6 hours for 4 days - reduces unfavourable outcomes and mortality |
| When should steroids not be given in suspected bacterial meningitis? | Post-surgical meningitis, severe immunocompromise, meningococcal or septic shock or those hypertensive to steroids |
| What is the contact prophylaxis regimens for bacterial meningitis? | Rifampicin for adults and children >12 (reduced efficacy of OCP, red colouration of urine and contact lenses) OR ceftriaxone IM as a single dose in adults |
| What vaccines are available against meningitis? | Neisseria meningitidis (serogroups A and C - travel vaccination, group C conjugate) - Haemophilus influenzae (HiB - noenates) - Strep pneumoniae (penumococcal vaccines) |
| What are the symptoms of rhabdomyolysis? | Triad of myalgia, muscle weakness and myoglobinuria |
| What are the clinical features of polymyositis? | Symmetrical, progressive proximal weakness developing over weeks to months - raised CK that responds to steorids |
| What are the clinical features of dermatomyositis? | Clinically similar to polymyositis - symmetrical, progressive weakness developing over weeks to months - but with associated skin lesions, "heliotrope rash" on face - up to 50% have underlying malignancy |
| What are the trigeminal autonomic cephalgias? | Primary headache disorders in the t rigeminal distribution - prominent ipislateral cranial autonomic features - cluster headache, paroxysmal hemicranias, SUNCT, hemicranias continua |
| What are the features of upper motor neurone lesions? | Drift of upper limb - weakness and loss of skilled movement (upper limb flexors > extensors, lower limb extensors stronger than flexors) - changes in tone and tendon/superficial reflexes - no muscle wasting |
| What are the changes in tone and tendon reflexes in upper motor neurone lesions? | Acutely - flaccid paralysis and loss of tendon reflexes | Later - increase in tone (spasticity), tendon reflexes become exaggerated |
| What are the changes in superficial reflexes in upper motor neurone lesions? | Normal flexor plantar response becomes extensor (+ve Babinski) | abdominal (and cremasteric) reflexes are abolished on the side affected |
| What are the three main patterns of upper motor neurone disorders? | Hemiparesis (wekaness of limbs on one side) - paraparesis (both lower limbs) - tetraparesis |
| What is the pattern of a UMN motor cortex lesions? | Weakness and/or loss of skilled movement confined to one contralateral limb (monoparesis - isolated motor cortex lesion) | defect in cognitive function (e.g. aphasia) and focal epilepsy may occur |
| What is the pattern of a UMN internal capsule lesion? | Small lesions cause large deficit - e.g. middle cerebral artery branch infarction produces a sudden, dense, contralateral hemiplegia |
| What is the pattern of a UMN pontine lesion? | Rarely confined to the corticospinal tract | adjacent strutures e.g. VIth and VIIth nuclei are involved - diplopia, facial weakness, internuclear ophthalmoplegia |
| What is the pattern of a UMN spinal cord lesion? | Isolated lesion of one lateral corticospinal tract causes an ipsilateral UMN lesion, the level indicated by changes in reflexes (e.g. absent biceps C5/6) - features of a Brown-Sequard syndrome and muscle wasting at the level of the lesion |
| What is the extrapyramidal system? | General term for basal ganglia motor systems - corpus striatum (caudate nucleus, globus pallidus + putamen), subthalamic nuclues, substantia nigra and parts of the thalamus |
| What features are present in extrapyramidal disorders? | Reduction in speed (bradykinesia) or akinesia (no movement) with muscle rigidity| involuntary movements (tremor, chorea, hemiballismus[unilateral, wildly,flinging], athotosis[involuntary writhing movements], dystonia[muscles contract uncontrollably]) |
| What is the classic manifestation os a cerebellar lesion? | Ataxia (unsteadiness) is characteristic |
| What side of the body do lateral cerebellar lobe lesions affect? | Ipsilateral side |
| Signs of cerebellar lesions? | DASHING - dysdiadochokinesia (impaired ability to perform rapid alternating movements, ataxia, speech (scanning, dysarthria), hypotonia, intention tremor, nystagmus, gait (ataxic - wide based) |
| What is titubation? | Rhythmic head tremor as either forward and back (yes-yes) movements or rotary (no-no) movements - mainly seen when cerebellar connections are involved |
| What is the role of the basal ganglia? | Facilitate purposeful movement, inhibit unwanted movements and have a role in posture and muscle tone |
| What are the characteristics of basal ganglia dysfunction? | Affect contralateral side of the body - lesions cause abnormal muscle control, changes in muscle tone and dyskinesias (including tremor, chorea and myoclonus) |
| What is the pathogenesis of Parkinson's disease? | Pars compacta region of the substantia nigra undergoes progressive neuronal degeneration - eosinophilic inclusion (Lewy) bodies develop | degeneration also occurs in basal ganglia nuclei | loss of dopamine in the striatum |
| What are the classical clinical features of Parkinson's disease? | TRAP - tremor (pill rolling) - rigidity (increased tone) - akinesia (loss or impairment of voluntary movement, bradykinesia, cogwheeling) - postural instability (stooping, shuffling gait,) |
| What are the risk factors for developing Parkinson's disease? | Old age (mean age of onset is 65) - family history - males more than females |
| What is cogwheeling? | Characteristically occurs in Parkinson's - stiffness with tremor - rigidity is broken up into a jerky resistance to passive movement |
| What cognitive changes can occur in Parkinson's disease? | Cognitive decline may occur early - dementia - depression is common |
| What other symptoms can occur in Parkinson's disease? | Ansomia, visual hallucinations, REM sleep disorder, constipation, heartburn, dribbling, dysphagia and weight loss, urinary difficulties, skin is greasy and sweating excessive |
| What is the course of Parkinson's disease? | Worsens over the years, slowly progressing, remissions are unknown |
| What are reflex changes in Parkinson's disease? | Reflexes are brisk - plantar reflexes ramin flexor |
| What investigations would you carry out in suspected Parkinson's disease? | Structural brain imaging (CT/MRI) - dopamine functional imaging (PET/DAT scan) - levodopa challenge (if they improve with levodopa then increased likelihood of Parkinson's? |
| What is the treatment of Parkinson's disease? | Levodopa and/or dopaminergic agonists produce striking improvement (increase dopamine) - only prescribe when symptomatic - give in combination with benserazide which reduces peripheral side effects, particulalry nausea |
| Does levodopa alter the natural progression of Parkinson's disease? | No |
| What are the unwanted effects of levodopa? | Nausea and vomiting, confusion, formed visual pseudo-hallucinations, chorea, after several years levodopa becomes ineffective, as treatment continues, episode of immobility develop, falls are common, chronic levodopa-induced movement disorder |
| What are some examples of dopamine receptor agonists and when are they used in Parkinson's disease? | (Pramipexole) Ropinirole is the usual drug of choice, as an alternative or addition to levodopa - less effective but have fewer later unwanted dyskinesias - use in those below 65 (levodopa for over 65) - vomiting common, haemolytic anaemia unusual |
| What are the clinical features and causes of drug induced parkinson's? | Tends to be symmetrical, coarse postural tremor | neuroleptics (phenothiazines, haloperidol) TCAs, | unwanted effects tend not to progress and settle when drugs are stopped |
| What are the clinical features of vascular parkinsonism? | Affects lower limbs - resting tremor is uncommon - poor levodopa response - signs of brain vascular lesions may be present (spasticity, hemiparesis, pseudobulbar palsy) |
| What are the signs of lower motor neurone lesions? | Seen in voluntary muscles - weakness, wasting, hypotonia, reflex loss, fasciculation, fibrillation potentials, muscle contractures, tropic changes in skin and nails |
| Where is pain of a spinal root compression felt? | In the myotome supplied by the root, also get tingling discomfort in the dermatome - pain is worse on manouveres that stretch the root or increase pressure in the spinal subarachnoid space |
| What are common causes of spinal root lesions? | Cervical and lumbar disc protrusions |
| What are the symptoms of a dorsal column lesion? | Vague - tingling, electric shock like sensations, clumsiness, numbness, band-like sensations - stamping gait - loss of vibration sense, light touch and proprioception - Lhermitte's sign (electric shock like sensations on neck flexion) |
| What are the symptoms of spinothalamic tract lesions? | Pure spinothalamic lesions cause contralateral loss of pain, pressure, coarse touch and temperature (2P's and 2 T's)sensation with a clear level below the lesion - dissociated sensory loss - i.e. painless burns - perforating ulcers and charcot joints |
| What are the three causes of acute compression of the spinal cord? | Cord transection (complete lesion) - Brown-sequard syndrome (hemisection) - central cord syndrome |
| What are the clinical features of central cord syndrome? | Hyperflexion or extension injury to already stenotic neck - predominantly upper limb weakness - "Cape" like spinothalamic sensory loss - lower limb preserved |
| What features predominant in chronic cord compression? | UMN signs - increased tone (spasticity), muscle weakness, increased reflexes - leads to spastic parapesis/tetra/quadri |
| What are the features of Brown-Sequard syndrome? | Contralateral loss of pain, pressure and temperature (spinothalamic) - ipsilateral loss of proprioception, vibration sense, two point discrimination and muscle function |
| From what levels does the spinal cord extend between? | C1-L1 where it becomes the conus medularis |
| What is the first palpable spinous process? | C7 |
| What are the five nerves of the brachial plexus? | Musculocutaneous (C5-7), Axillary (C5-T1), Median (C5-T1), Radial (C5-T1) , Ulnar (C8-T1) |
| What is the blood supply of the spinal cord? | Anterior spinal artery and a plexus on the posterior cord |
| What are some causes of spinal cord compression? | Spinal cord neoplasm - TB - disc and vertebral lesion - spinal epidural abscess, epidural haemorrhage and haematoma |
| What is syringomyelia? | Progressive expansion of a fluid cavity in the spinal cord (cervical/thoracic)- may be due to congenital causes, tumour ot trauma - classically causes spinothalamic loss where the cavity occupies the central cord |
| What is the management of a spinal cord compression? | MRI shows cord pathology - plain film for bony pathology - surgical exploration is often necessary - decompression - if not infective give steroids§ |
| What is syringobulbia? | Fluid filled cavity in the branstem? |
| What is a Arnold-Chiari malformation? | Cerebellum herniates through foramen magnum - frequently associated with syringomyelia |
| What are the clinical features of syringomyelia? | Upper limb pain is exacerbated by exertion/coughing - dissociated spinothalamic loss (pain, pressure, temperature, coarse touch) - loss of upper limb reflexes, muscle wasting in hand and forearm, spastic parapesis, neuropathic joints, trophic skin changes |
| What are the clinical features of syringobulbia? | Brainstem signs - tongue atrophy and fasciculation, bulbar palsy, nystagmus, Horner's syndrome, hearing loss and impairment of facial sensation |
| What are the investigations/management or syringomyelia/syringobulbia? | MRI demonstrates cavity and herniation - gradually progressive - no curative treatment, sudden deterioration can occur - surgical decompression at foramen magnum sometimes slows deterioration |
| What is the most common metabolic cause for spinal cord damage? | Vitamin B12 deficiency - may also have megaloblastic anaemia, other neurological changes: mental slowing, cerebellar ataxia & peripheral neuropathy |
| What is lathyrism? | An endemic spastic parapesis of central India |
| What is konzo? | Tropical ataxic neuropathy - West Africa and Caribbean - subacute spastic parapesis or quadripesis - sensory ataxia, loss of reflexes, deafness and optic neuropathy |
| What is acute transverse myelopathy? | A cord lesion and parapesis (or paraplegia) occurring with viral infections, MS, mixed connective tissue disease and other inflammaotry and vascular conditions - MRI required to exclude cord compression |
| When may anterior spinal artery occlusion occur? | Thrombotic or embolic vascular disease (endocarditis, severe hypotension, atheroma, diabetes mellitus, polycythaemia, syphilis and polyarteritis) - sometimes during surgery, or follows aortic dissection and trauma - isolated event |
| What is the management of paraplegia? | Any intercurrent infection is potentially dangerous and should be treated early - chronic renal failure most common cause of death - catheterisation - acute bowel evacuation - skin care (sores) - passive physiotherapy (prevent contractures) - rehab |
| What is motor neurone disease? | Progressive deterioration of lower and upper motor neurones in the psinal cord, in cranial nerve nuclei and within the cortex - degeneration of the motor cortex and anterior horns of the spinal cord |
| What is the epidemiology of motor neurone disease? | Slight male predominance, onset occurs typically in the over 50's |
| What are the four classifications/causes of motor neurone disease? | Amyotrophic lateral sclerosis (ALS) 70% - progressive bulbar palsy 20% - progressive muscular atrophy 5% - primary lateral sclerosis 5% |
| What are the clinical features of amyotrophic lateral sclerosis? | Disease of the lateral corticospinal tracts - muscle atrophy - progressive spastic tetra/parapesis with added LMN signs and fasciculations - weeks to months - painless wasting without sensory loss - assymetrical isolated weakness - "mixed signs" |
| What are the investigations for amyotrophic lateral sclerosis? | Neurophysiology (EMG with evidence of fasciculations) - MRI brain and spine to exclude other causes - CK to exclude myopathy - overnight pulse oximetry and ABG |
| What are the clinical features of progressive muscular atrophy? | Wasting beginning in the small muscles of one hand (or both), spread inexorably - wasting follows on both sides - fasciculation is common - cramps may occur - weakness - often widespread - tendon reflexes are lost - sphincter disturbances occur late |
| What are the clinical features of progressive bulbar and pseudobulbar palsy? | Lower cranial nerve nuclei and their supranuclear connections initially (CN IX-XII)- dysarthria, dysphagia, nasal regurgitation of fluids and choking are common- women>men - Bulbar & pseuedo palsy: e.g. wasted fibrillating tongue with spastic weak palate |
| What are the clinical features of primary lateral sclerosis? | Loss of betz cells - least common form - confined to UMN - progressive tetraparesis with terminal pseudobulbar palsy |
| How is a diagnosis of motor neurone disease made? | Largely clinical - denervation (except PLS) is confirmed by EMG: chronic partial denervation with preserved motor conduction velocity - CSF normal |
| What is Kennedy's syndrome? | X linked bulbar and spinal muscular atrophy - unulateral, ipsilaterl optic atrophy - contralateral papilloedema 2nd to raised ICP - central scotoma - anosmia - upper motor signs are not seen - memory loss, nausea & vomiting |
| What is the course of motor neurone disease? | Remission is unknown - progresses, spreading gradually, and causes death (often from bronchopneumonia) - survival for more than 3 years is unusual |
| What is the treatment of motor neurone disease? | Riluzole (Na channel blocker, inhibits glutamate release) slows progression slightly (extra 3 months of life) - spasticity may be helped by baclofen - amitriptyline/propantheline for drooling - ventilator support and feeding by gastrotomy helps prolong |
| What is the definition of dementia? | Progressive decline of cognitive function, usually affecting the cortex as a whole, though sometimes patchily |
| What are the clinical features of dementia? | Memory is especially affected, intellect gradually falls - loss of emotional control, deterioration of social behaviour and loss of motivation |
| What is the epidemiology of dementia | 10% of those over 65, 20% of those over 80 |
| What are the most common causes of dementia? | Alzheimer's, fronto-temporal, vascular and dementia with lewy bodies |
| What is the commonest form of dementia? | Alzheimer's - accounts for over 65% of dementia in any age group |
| What are the clinical features of Alzheimer's? | Progressive memory loss - decline in language - apraxia (loss of skilled motor tasks) - agnosia (failure to recognise objects) - progressive loss of executive function (organising, planning and sequencing) - behavioural change (agitation)- loss of insight |
| What brain changes are seen on imaging? | Decreased size of brain, widening of sulci, narrowing of gyri - compensatory dilatation of ventricles, secondary hydrocephalus |
| What is the onset and course of Alzheimer's like? | Gradual onset - progressive course over 10+ years, with death in a state of extreme cognitive decline |
| What late changes occur in Alzheimer's? | Disturbances of gait, motor and occasionally sensory abnormalities |
| What is the neuropathology in Alzheimer's disease? | Loss of neurones with astrocytosis - neurofibrillary tangles (in cell bodies, tau protein with ubiquitin) - senile plaques (extracellular, beta-amyloid) - amyloid angiopathy - seen in frontal, temporal, parietal cortex, hiipocampi etc - apoptosis follows, |
| What are the neurochemical changes in Alzheimer's disease? | Marked reduction in choline transferase, acetylcholine, noradrenaline and serotonin |
| What are the clinical features of dementia with Lewy bodies? | Dementia predominating feature - daily fluctuations in alertness, attention & cognition - prominent memory loss may not occur early - depression and sleep disorders occur - recurrent formed visual hallucinations are common - Parkinsonism with falls |
| What is the pathology of dementia with Lewy bodies? | Degeneration of the substantia nigra, the remaining nerve cells contain abnormal structures called Lewy bodies (hallmark) - detected by staining for uniquitin |
| How common is dementia with Lewy bodies? | 25% of dementias |
| What are the features of extreme sensitivity to neuroleptic medication in patients with dementia with Lewy bodies? | Up to 50% - worsening cognition, heavy sedation, increased or possibly irreversible parkinsonism, or symptoms resembling neuroleptic malignant syndrome (NMS), which can be fatal. (NMS causes severe fever, muscle rigidity and breakdown -KF) |
| What is the clinical course of vascular dementia? | Can be sudden onset & step-wise deterioration |
| What features are seen on MRI in vascular dementia? | Widespread vessel disease - could be one large infarct too |
| What are the characteristic features of Pick's disease? | Slowly progressing changes in character, personality and social deterioration leading to impairment of intellect, memory, speech and communication - changes in eating habits - lower attention span - usually presents earlier (50-60) - frontal & temporal |
| What are the clinical features of vascular dementia? | Can depend on the area of infarct |
| What is the course of Pick's disease? | Mean length is 7 years - rapidly progressive |
| What is the neuropathology of Pick's disease? | Pick's cells (swollen neurons) and intracytoplasmic filamentous inclusions known as Pick's bodies - neuronal loss and astrocytosis |
| What are the clinical features of frontotemporal dementia? | Progressive deterioration of social behaviour, disinhibition and personality develops in middle life, followed by decline in memory, intellect and language |
| What is the classification of Pick's disease? | A type of fronto-temporal dementia |
| How common is fronto-temporal dementia? | 3% of dementias |
| What will imaging show in fronto-temporal dementia? | Selective atrophy of frontal and temporal lobes |
| What pathological changes are seen in fronto-temporal dementia? | No excess of senile plaques or neurofibrillary tangles - cytoplasmic inclusion bodies (silver staining) - Pick's bodies are seen |
| What are some examples of rarer causes of dementia? | idiopathic Parkinson's, Huntington's, Creutzfeldt-Jakob, Wilson's, Whipples, late stages of MS |
| What investigations would you do in dementia? | History and basic examination - cognitive testing - collateral history - imaging: MRI, PET - if younger then: EEG, CSF exam and brain biopsy |
| What is the management of dementia? | Rare that treatable cause is found - supportive, preserve dignity - anticholinesterase inhibitors (donepezil, rivastigmine and galantamine) or memantine (NMDA receptor antagonist) may slightly slow rate of cognitive decline |
| What is cerebral palsy? | Chronic disorder of posture and movement caused by non-progressive CNS lesions sustained before 2 years old resulting in delayed motor development, evolving CNS signs, learning disability & epilepsy |
| What are examples of causes of brain damage in children? | Most are antenatal events unrelated to birth trauma - hypoxia, cerebral haemorrhage and/or infarction, trauma, prolonged seizures (status epilepticus), hypoglycaemia |
| What is athetosis? | Continuous succession of slow, writhing, involuntary movements of the hands and feet and other body parts |
| What are the clinical features of cerebral palsy? | Failure to achieve normal milestones - weakness, paralysis, seizures, language/speech problems - specific motor syndromes - spastic diplegia - athetoid - infantile hemiparesis - congenital ataxia |
| What is the management of cerebral palsy? | Physio - speech and language - OT - botox - selective surgery - orthotic devices - |
| What is dysraphism? | Failure of normal fusion of the foetal neural tube leads to a group of congenital abnormalities |
| What are the causes of dysraphism? | Folate deficiency during pregnancy is a contributor - antiepileptic drugs (valproate) are also implicated |
| What are the signs/symptoms of dysraphism? | Anencephaly - meningoencephalocele - spina bifida - spina bifida occulta - meningomyelocele |
| What is anencephaly? | Absence of a major portion of the brain, skull and scalp - during embryonic development |
| What is meningoencephalocele? | Brain and meninges extrude through a midline skull defect - can be minor or massive |
| What is spina bifida? | Failure of lumbosacral neural tube fusion |
| What is spina bifida occulta? | Isolate failure of vertebral arch fusion (usually lumbar), often seen incidentally on x rays - dimple or tuft of hair may overlie the anomoly |
| What is a meningomyelocele? | Elements of spinal cord and lumbosacral roots within a meningeal sac - this herniates through a vertebral defect - if severe can lead to lower limb and spincter paralysis - should be closed within 24 hrs of birth |
| What is a platybasia? | A congenital anomaly - malformed relationship between the occipital bone and cervical spine - upward invagination of the foramen magnum and skull base - lower cranial nerves, medulla, upper c cord and roots are affected |
| What are the features of neurofibromatosis type 1? | Multiple skin neurofibromas and pigmentation (cafe au lait patches), freckling in skin folds - arise from nerilemmal sheath - autosomal dominant (complete penetrance) - plexifrom neurofibromas on major nerves & proximal nerve roots, sometimes spinal cord |
| What is the management and treatment of neurofibromatosis type 1? | Yearly measurement of blood pressure and cutaneous survey - surgical removal is pressure symptoms develop |
| What are the clinical features of neurofibromatosis type 2? | Many neural tumours occur and some associated abnormalities |
| What is more common neurofibromatosis type 1 or 2? | Type 1 |
| What neural tumours occur in neurofibromatosis type 2? | Many neural tumours occur: meningioma, (bilateral) acoustic (CN VIII) schwannoma (sensinoneural loss), glioma (including optic nerve), plexifrom neuroma, cutaneous neurofribroma |
| What associated abnormalities can occur in neurofibromatosis type 2? | Scoliosis, orbital haemangioma, local gigantism of a limb, phaechromocytoma and ganglioneuroma, renal artery stenosis, pulmonary fibrosis, obstructive cardiomyopathy, fibrous dysplasia of bone, cafe au lait patches |
| What is the treatment of neurofibromatosis type 2? | Tumours causing pressure symptoms within the nervous system require excision if feasible |
| What is the inheritance of neurofibromatosis type 2? | Autosomal dominant - 50% occur de novo |
| What are the clinical features of tuberous sclerosis? | Congenital - shagreen patches ("shark skin") - ash leaf macules on skin - adenoma sebaceum (butterfly on face) - epilepsy - cognitive impairment (decreased IQ) - haemartoma formation - retinal phakomas (glial masses) - renal tumours |
| What is the inheritance of tuberous sclerosis and how common is it? | Rare - autosomal dominant |
| What are the clinical features of Sturge-Weber syndrome? | Congenital - xtensive port-wine naevus on one side of face (usually 5th nerve distribution) with meningeal angioma - focal epilepsy - vascular eye abnormalities |
| What genes are involved in tuberous sclerosis and what do they code for? | TSC 1 and 2 - which code for the proteins hamartin and tuberin (usually tumour growth suppressors) |
| What is the treatment for Sturge-Weber syndrome? | Laser therapy - lamotrigine/carbamazepine for epilepsy |
| What are the features of Von Hippel-Lindau syndrome? | Autosomal dominant - retinal and cerebeller haemangioblastomas (cord, cerebellum, renal) - visual impairment, ataxic, dizziness, weakness, hypertension |
| What is Friedrich's ataxia? | Autosomal recessive progressive degeneration of dorsal root ganglia, spinocerebellar tracts, corticospinal tracts and cerebellar Purkinje cells - abnormal function of mitochondrial ATP |
| What are the clinical features of Friedrich's ataxia? | Ataxia of gait and trunk, nystagmus, dysarthria, absent lower limb position and vibration sense, absent lower limb reflexes, optic atrophy, pes cavus, cardiomyopathy |
| What are the two main cellular structures of peripheral nerves? | Nerve nucleus with its axon - myeline sheath, produced by Schwann cells between each node of Ranvier |
| What is the blood supply to peripheral nerves? | Via the vasa nervorum |
| What are the mechanisms of nerve damage? | Demyelination, axonal degeneration, Wallerian degeneration, compression, infarction and infiltration |
| What occurs in demyelination? | Schwann cell damage leads to myelin sheath disruption - causes marked slowing of conduction |
| What occurs in axonal degeneration? | Axon damage leads to nerve fibre dying back from the periphery - conduction velocity remains norma initially (axonal continuity in surviving fibres) - occurs typically in toxic neuropathies |
| What occurs in Wallerian degeneration of peripheral nerves? | Describes change following nerve section - both axon and distal myelin sheath degenerate over several weeks |
| What occurs in peripheral nerve compression? | Focal demyelination at the point of compression causes disruption in myelin sheath - typically in entrapment neuropathies |
| What occurs in peripheral nerve infarction? | Microinfarction of vasa nervorum - occurs in diabetes and arteritis - Wallerian degeneration occurs distal to the ischaemic zone |
| What occurs in peripheral nerve infiltration? | Infiltration of peripheral nerves by inflammatory cells - occurs in leprosy and granulomas (e.g. sarcoid) |
| How does peripheral nerve regeneration occur? | Either by remyelination (Schwann cells) or by axonal growth down the nerve sheath (sprouting from axonal stump) |
| What is the definition of neuropathy? | Pathological process affecting a peripheral nerve or nerves |
| What is the definition of mononeuropathy? | Pathological process affecting a single nerve |
| What is the definition of mononeuritis multiplex? | Pathological process affecting several or multiple nerves |
| What is the definition of polyneuropathy? | Diffuse, symmetrical disease, usually commencing peripherally - course may be acute, chronic, static, progressive, relapsing or towards recovery - are motor, sensory, sensorimotor and autonomic - classified broadly into demyelinating and axonal |
| What nerves are affected first in peripheral neuropathy? | Long fibres - get length dependent pattern (glove and stocking) |
| What are the clinical features of a polyneuropathy? | Widespread loss of tendon reflexes is typical, with distal weakness and distal sensory loss |
| What is the definition of a radiculopathy? | Disease affecting nerve roots and plexopathy (brachial or lumbosacral) - disc protrusion commonly |
| What is the definition os a myelopathy? | Disease of the cord |
| What nerve is affected in carpal tunnel syndrome and what are its roots? | Median nerve - C6-T1 |
| What diseases is carpal tunnel syndrome commonly seen in? | Hypothyroidism, diabetes, pregnancy (third trimester 10%), obesity, rheumatoid disease, acromegaly, amyloid, renal dialysis patients, wrist trauma |
| What are the clinical features of carpal tunnel syndrome? | Nocturnal tingling and pain in the hand and/or forearm followed by weakness of the thenar muscles - sensory loss in the palm and radial 3 1/2 fingers develops - wasting of abductor pollicis brevis - tinnels sign and phalens' sign positive |
| What are tinnel's and phalen's sign and what disease would they be positive in? | Tinnel's - percussion of the median nerve at wrist to provoke parasthesiae | Phalen's - dorsiflexion of wrist for 30-60s | carpal tunnel syndrome |
| What are the treatment options for carpal tunnel syndrome? | Wrist splint at night or local steroid injection in the wrist gives relief in mild cases - in pregnancy it is self-limiting - reducing obesity helps too - surgical decompression is definite treatment |
| What nerve is affected in cubital tunnel syndrome and what are its roots? | Ulnar nerve - C7-T1 |
| What are the clinical features of ulnar nerve compression? | Weakness and wasting of the ulnar innervated muscles leads to clawing of the hand - hypothenar muscles, interossei and medical two lumbricals - with sensory loss in the ulnar one and a half fingers |
| What is used for diagnosis of peripheral nerve compression and entrapments? | Nerve conduction studies |
| What is the treatment of ulnar nerve compression? | Decompression and transposition of the nerve at the elbow is sometimes helpful - rest and avoiding pressure - elbow splint at night |
| Where else can the ulnar nerve get entrapped other than the cubital tunnel? | Guyan's canal - deep, solely motor branch of ulnar nerve is damaged in the palm from repeated trauma (ie. from crutch, screwdriver handle or cycle handlebars) |
| What are the roots of the radial nerve and what is its general function? | C5-T1 - opens the fist |
| Where does the radial nerve get compressed and what are the clinical features? | Compressed acutely against the humerus (fractured humerus, arm draped over hard chair for hours ("Saturday night palsy") - wrist drop and weakness of brachioradialis and finger extension follow - anatomical snuff box sensation affected |
| What other upper limb nerve compression causes wrist drop? | POsterior interosseus nerve in the forearm leads to wrist drop without weakness of brachioradialis |
| What are the roots of the common peroneal (fibular) nerve, where does it get compressed and what are the clinical features? | L4-S1 - head of fibula - prolonged squatting, yoga, pressure from cast, prolonged bed rest - foot drop and weakness of ankle eversion - ankle jerk preserved - numbness on anterolateral border of dorsum of foot and/or lower shin - recover within months |
| What condition is mononeuritis multiplex highly suggestive of? | Vasculitis - 2 or more peripheral nerves |
| What is Guillain-Barre syndrome? | Acute autoimmune inflammatory demyelinating polyneuropathy - paralysis follows 1-3 weeks after an infection that is often trivial and seldom identified (Campylobacter, CMV, zoster, HIV, EBV, vaccinations) - antibody response against peripheral nerves |
| What are the clinical features of Gullain-Barre syndrome? | Paralysis follows 1-3 weeks after infection- weakness of distal limb muscles and or distal numbness - symptoms progress proximally (days-6 weeks) - loss of tendon reflexes - peak symptoms 10-14 days - monophasic (doesn't recur) |
| How is the diagnosis of Gullain-Barre syndrome made? | Clinical grounds - nerve conduction (slowing and/or block) - CSF protein raised - antiganglioside antibodies - examination may be normal initially |
| What is the prognosis in Gullain-Barre if there is complete paralysis? | It is compatible with complete recovery! |
| What is the management of Gullain-Barre syndrome? | Ventilator support - subcutaneous heparin to reduce risk of venous thrombosis - IV immunoglobulin within first 2 weeks as reduces duration and severity (screen for IgA deficiency before) - no steroids |
| What is the course of Gullain-Barre syndrome? | Imrpovement towards independent mobility is gradula over many months but may be incomplete |
| What is chronic inflammatory demyelinating polyradiculopathy (CIDP)? | Autoimmune demyelinating disease of peripheral nerves |
| What are the clinical features of CIDP? | Develops over weeks or months, usually relapsing and remitting, but generally persists long term - distal onset of weakness & sensory loss in limbs, with peripheral nerve enlargemenet and increased CSF protein |
| What features would you find investigation of CIDP? | Some cases have plaques resembling MS lesions - CSF protein is raised - segmental demyelination in nerve biopsy |
| What is the treatment of CIDP? | Responds to long-term, low dose steroids and to IV immunoglobulin (used for exacerbations) |
| What is the course of CIDP? | With drug therapy - most CIPD cases run a mild course over many years |
| What are the clinical features of diphtheritic neuropathy? | Palatal weakness followed by pupillary paralysis and a sensorimotor neuropathy occur several weeks after the throat infection |
| What neuropathies can occur in diabetes mellitus? | Symmetrical sensory polyneuropathy - acute painful neuropathy - mononeuropathy and multiple mononeuropathy (cranial nerve lesions or isolate peripheral nerve lesions (e.g. Carpal tunnel syndrome) - diabetic amytrophy - autonomic neuropathy |
| What neuropathy is sometimes seen in thyroid disorders? | A mild chronic sensotimotor neuropathy |
| What are the clinical features of porphyria? | Episodes of a severe, mainly proximal neuropathy in the limbs, sometimes with abdominal pain, confusion (acute psychosis) and coma - alcohol, barbiturates and intercurrent infection can precipitate attacks |
| What are the clinical features of alcohol neuropathy? | POlyneuropathy, mainly lower limbs, calf pain is common - repsonse to thiamine is variable - recurrence and progression occur with even small amounts of alcohol |
| What is Wernicke-Korsakoff syndrome? | Thiamine-responsive encephalopathy due to ischaemic damage in the brainstem and its connections |
| What are the clinical features of Wernicke-Korsakoff syndrome? | Eye signs (nystagmus, CN VI palsy, fixed pupils, papilloedema) - ataxia (broad-based gait) - cognitive changes (amnestic syndrome, confabulation, restlessness, stupor and coma) - delirium tremens - hypothermia and hypotension (hypothalamic involvement) |
| What is the treatment of Wernicke-Korsakoff syndrome? | Thiamine parenterally - give slowly as risk of anaphylaxis, otherwise harmless - untreated leads to an irreversible amnestic state |
| What is Charcot-Marie-Tooth disease and what are the clinical features? | Hereditary| distal limb wasting and weakness (typically motor) - slowly progresses (starts in puberty) |mostly legs |variable loss of sensation and reflexes| when advanced, legs resemble inverted champagne bottle| palpable nerve| pes cavus & toe clawing |
| What is the management of Charcot-Marie-Tooth disease? | Incurable - may respond to nerve release |
| What is POMES syndrome? | Chronic inflammatory demyelinating Polyneuropathy, Organomegaly (liver), Endocrinopathy (gynaecomastia and atorphic testes), M protein band and Skin hyperpigmentation |
| What occurs in critical illness polyneuropathy? | 50% of patients with multiple organ failure and/or sepsis develop an axonal polyneuropathy - inflammatory response impairs neural metabolism - distal weakness and absent reflexes during recovery - resolution is usual |
| What is myasthenia gravis? | Most common disorder of the neuro-muscular junction - acquired, probably heterogenous - twice as common in females - reduced function of ACh receptors and inflammation |
| What are the clinical features of myasthenia gravis? | Fatiguability of proximal limb, extraocular (ptosis), speech, facial expression and mastication muscles - respiratory difficulties - fluctuating, fatiguable weakness - muscle pain absent - wasting sometimes after many years |
| What antibodies are found in myasthenia gravis? | anti-AChR antibodies (acetylcholine receptor) commonly found (immune complexes and complement are depositied at the postsynaptic membrane) - anti-MuSK (muscle-specific receptor tyrosine kinase (in anti-AChR negative cases) |
| What investigations should be done in myasthenia gravis? | Serum anti-AChR and anti-MuSK antibodies - repetitive nerve stimulation - tensilon (edrophonium) test, when positive get substantial improvement in weakness within seconds lasting for up to 5 minutes - mediastinal MRI - other antibodies |
| What is the course and management of myasthenia gravis? | Fluctuates - most are protracted & life long - emergency assisted ventilation may be required - exacerbations are usually unpredictable and unprovoked |
| What is the treatment of myasthenia gravis? | Oral anticholinesterases: pyridostigmine - helps weakness, muscarinic side effects (^salivation/diarrhoea) give oral atropine too | immunosuppressants: 2nd line - prednisolone, azathioprine| thyectomy | plasmapharesis and IV Ig during exacerbations |
| What is the management of polyneuropathies? | Treat cause - physio and OT - foot care and shoe choice - IV immunoglobulin Gullain Barre and CIDP - steroids/immunosuppressants if vasculitic - amitriptyline/gabapentin for neuropathic pain |
| How would you clinically test for fatiguability (MG)? | Eyes: maintain upgaze for 30 secs - Bulbar: observe speech and dysarthria in a prolonged conversation (counting) - Arms: compare shoulder abduction on both sides |
| What conditions are associated with myasthenia gravis? | Thymic hyperplasia (in 70% below 40) - 10% have thymic tumour - thyroid disease, rhuematoid disease, pernicious anaemia and SLE |
| When is the peak incidence of myasthenia gravis? | Women in their 3rd decade, men in their 6th or 7th decade |
| What is Lambert-Eaton myasthenic-myopathic syndrome (LEMS)? | Paraneoplastic manifestation of small-cell bronchial carcinoma (can be breast, prostate, stomach, lymphoma too) due to defective acetylcholine release at the NMJ |
| What are the clinical features of LEMS? | Proximal limb muscle weakness, rarely with ocular/bulbar, some absent tendon reflexes - weakness tends to improve after a few minutes of contraction and absent reflexes return - gait difficulties before eyes - dry mouth (autonomic) |
| How is a diagnosis of LEMS made? | EMG and repetitive stimulation (low amplitude muscle action potentials and increment at high stimulation frequency) - antibodies to P/Q type voltage gated calcium channels in 90% |
| What is the treatment of LEMS? | Diaminopyridine (DAP) is a safe and effective treatment |
| What are the two x-linked recessive muscular dystophies? | Duchenne's and Becker's muscular dystrophies |
| What protein is missing in Duchenne/Becker's muscular dystrophy? | Dystophin is absent in Duchenne's, whilst in Becker's it is present but levels are low (less severe form of Duchenne's) - essential for cell membrane stability, reduction in glycoproteins in the DAP complex that link dystrophin to laminin |
| What are the clinical features of Duchenne's muscular dystrophy? | Delay in motor development, obvious by 4 - waddling, clumsy gait - Gower's sign on rising (uses hands to climb up his legs) - proximal limb weakness, calf psuedohypertrophy - developmental delay - "shoulder back, belly out" - affected myocardium |
| What is the prognosis of Duchenne's muscular dystrophy? | Severe disability by the age of 10 - death by 20 (respiratory and cardiac involvement) |
| What are the clinical features of Becker's muscular dystrophy? | Later onset than Duchenne's, slower progression, increased calf psuedohypertrophy |
| What investigations would you do in Duchenne's/Becker's muscular dystrophy? | Diagnosis is usually suspected clinically - serum CK grossly elevated - biopsy shows variation in muscle fibre size, necrosis, regeneration and replacement by fat, immunochemical staining shows absence of dystophin - EMG shows myopathic pattern |
| What is the management in those with x linked recessive muscular dystrophies? | No curative treatment - passive physiotherapy helps contractures - portal respiratory support - carrier detection - genetic advice (determination of foetal sex and selective abortion) |
| What is a myotonia? | Continued, involuntary muscle contraction after cessation of voluntary effort - cause tonic muscle spasm |
| What is myotonic dystrophia? | Commonest muscular dystrophy - autosomal dominant - progressive muscle weakness - ptosis, cataracts, weakness and thinning of face, frontal baldness, mild cognitive impairment - 20-50 yrs - phenytoin or similar helps myotonia |
| What is consciousness? | Wakefulness with awareness of self and surroundings |
| What is clouding of consciousness? | Reduced wakefulness and/or self-awareness, sometime with confusion |
| What is confusion? | Subject is bewildered and misinerprets their surroundings |
| What is delirium? | State of confusion, sometimes with visual hallucination and often high arousal |
| What is sleep? | Normal mental and physical inactivity - subject can be aroused |
| What is stupor? | Abnormal - sleep state from which the subject can be roused by vigorous or repeated stimuli |
| What is a coma? | Unrousable unrespobsiveness |
| What two separate anatomical and physiological systems does consciousness depend on? | Ascending reticular activating system (ARAS): determines arousal | cerebral cortex: determines the context of consciousness |
| What are the components of the Glasgow coma scale? | Designed for recording coma following head injuries - Eye opening (4 spontaneous, speech, pain, 1 no response) - Motor response (6 obeys, localises, withdraws, flexion, extension, 1 no response) - Verbal response (5 orientation->1 no response) |
| What three mechanisms can cause coma? | Diffuse brain dysfunction (generalised severe metabolic or toxic disorders) - direct effect within the brainstem (inhibits reticular formation) - pressure effect on the brainstem (mass lesion, inhibits reticular formation) |
| What are the two types of sleep? | Non-rapid eye movement and rapid eye movement |
| What occurs during non-REM sleep? | More at start of night - 3/4 of sleep for young adults - synchronised, thythmiic EEG activity, decreased cerebral blood flow (reduced HR, BP and TV), partial muscle contraction - some non-narrative images - more important: brain recovery |
| What occurs during REM sleep? | Mostly at end of night - EEG shows fast activity, increased brain activity (fMRI) and increased cerebral blood flow (impaired thermal regulation), completely relaxed muscles - narrative dreaming - mainly for early brain development - consolidates memory |
| What are the 3 mechanisms of sleep? | Homeostatic: tired, body tries to sleep - emotional response: despite tiredness your kept awake (exam stress) - circadian rhythm: naturally more tired at 4am and 2pm |
| What is insomnia? | Fitful sleep - less time than usual spent in REM sleep - rarely a feature of neurological disease - ask "do you experience difficulty sleeping?" & "do you have difficulty falling/staying asleep?" |
| What is parasomnia? | Sleep paralysis - abnormal movements, behaviours, emotions, perceptions & dreams - may see alien at foot of bed |
| What is narcolepsy? | People fall asleep suddenly at inappropriate times - chronic autoimmune disease, inhibits brains ability to regulate sleep/wake times - daytime sleepiness -cataplexy (sudden muscle weakness) -hallucinations - sleep paralysis -overnight PSG, LP, sleep test |
| How much sleep is required? | 7-7.5 hours is enough - mid-afternoon nap of 15 minutes is equivalent to 90 minutes overnight - in old age sleep requirements fall, sometimes 4 hours a night but may nap more |
| What is a normal CSF glucose value? | 60-70% of blood glucose |
| What can cause a brain abscess? | Either local spread of infection or secondary to a remote infective process - chronic ear infection, sinusitis, dental infection, post-trauma, post-neurosurgery |
| What are the clinical features of a brain abscess? | Classical triad: fever, headache, focal neurological signs - ± seizures |
| What organisms cause brain abscesses? | Streptococci (particulalry S. milleri), Coliforms (proteus sp), anaerobes, Staph. aureau, Actinomyces sp. |
| How is a brain abscess diagnosed? | CT brain |
| What is the treatment of a brain abscess? | Drain the pus and antibiotics (ceftriaxone and metronidazole) for 6 weeks |
| What is a stroke? | A syndrome of rapid onset of cerebral deficit (usually focal) lasting >24hr or leading to death, with no cause apparent other than vascular |
| What is the most treatable risk factor for stroke? | Hypertension |
| What are the two types of stroke? | Haemorrhagic: blood leaks into blood tissue (17%) - Ischaemic: clot stops blood supply to an area of brain (80%) |
| What are the causes of haemorrhagic stroke? | Primary intracerbral haemorrhage: hypertension, amyloid angiopathy | secondary intracerebral haemorrhage: Av malformation, aneurysm, tumour | subarachnoid haemorrhage |
| What are the causes of ischaemic cerebrovascular stroke? | Thrombosis, large artery stenosis, small vessel disease, cardio-embolic stroke, hypoperfusion |
| What are the scores used in Rosier score and what syndrome is it used to assess? | Stroke - loss of consciousness or syncope (-1), seizures (-1), new assymetrical facial (+1), arm(+1), leg(+1) weakness, speech disturbance (+1), visual field defect (+1) - score > 0 is likely to be a stroke |
| What are the risk factors for stroke and how can they be managed? | Aspirin in those with 10-year risk of coronary heart disease > 10% - hypertension: treat & monitor - smoking: stop - lifestyle: active - alcohol: moderate intake - cholesterol: statins - haematocrit: reduce - AF: anticoagulate - obesity - diabetes |
| What are the different sizes of stroke? | Total anterior circulation syndroem - partial anterior circulation syndrome - lacunar syndrome - posterior circulation syndrome - TACS, PACS, LACS & POCS |
| What are the clinical features of a total anterior circulation syndrome (TACS)? | Middle meningeal artery blocked, affects all white & grey matter in that distribution - hemiplegia with at least two of face, arm and leg ± hemisensory loss - homonymous hemianopia - dysphagia (cortical signs) - most serious, only 5% independent at 1 year |
| What are the clinical features of a partial anterior circulation syndrome (PACS)? | Only some grey matter affected in middle meningeal distribution - 2/3 features present in TACS (hemiplegia of face, arm or leg) or isolated cortical dysfunction (dysphagia) or pure motor - 55% independent at 1 year |
| What are the clinical features of a posterior circulation syndrome (POCS)? | Mixed bag of things - Cranial nerve palsy AND contralateral motor/sensory defect Bilateral motor or sensory defect Eye movement problems (e.g.nystagmus) Cerebellar dysfunction Isolated homonymous hemianopia |
| What are the clinical features of a lacunar syndrome (LACS)? | Just deep white matter disease, in particular motor tracts of internal capsule - affects 2 of face, arm and leg - most commonly purely motor - best prognosis, 60% independent at 1 year |
| What would be affected if the stroke was right sided? | Right brain for relating things spatially - left side of body affected - creativity, music, spatial orientation, artistic awareness |
| What would be affected if the stroke was left sided? | Left brain for relating things in a linear manner - right side of body affected - spoken language, number skills, reasoning, written language |
| What is the ischaemic penumbra? | Area around necrotic core of tissue that is still viable due to collateral blood flow |
| What are the initial signs of a stroke? | FAST - Face: fallen on one side? - Arms: can they raise them and keep them there? - Speech: slurred? -> Time to call 999 |
| What is the initial management of a stroke? | Imaging: CT (dense artery sign, loss of grey/white differentiation), MRI - if imaging excludes haemorrhage give alteplase therapy(can be given up to 4.5hrs after symptom onset) (aspirin if thrombolytic therapy is contraindicated) - neurosurgical for H |
| What is the longterm management of a stroke? | Rehab - antihypertensive therapy - antiplatelet therapy: aspirin for 10-14 days, after 14 days either: clopidogrel or aspirin + dipyridamole - statins - anticoagulants |
| How is thrombotic risk assessed and what thromboprophylaxis is used? | CHADS2: Congestive cardiac failure, hypertension, age (75+), diabetes, previous stroke (x2) - low risk: nothing or aspiring - medium risk: oral anticoagulant (warfarin or rivaroxaban) or aspirin - high risk: oral anticoagulant |
| What is a TIA? | Transient ischaemic attack - transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia without acute ischaemia - <24hrs - tendency to recur and may herald thromboembolic stroke - usually microemboli |
| What is amurosis fugax? | Sudden transient loss of vision in one eye (curtain coming down) - arterial obstruction sometimes visible through opthalmascope - first clinical evidence of internal carotid artery stenosis - can be benign - diplopia, vertigo, vomiting |
| What is transient global amnesia? | Episodes of amnesia/confusion lasting several hours - 65+ - complete recovery - presumed to be due to posterior circulation ischaemia |
| What are the clinical findings in a TIA? | Consciousness is usually preserved - unusual to witness an attack as so brief - clinical evidence of a source of embolus: carotid artery bruit (stenosis), AF or other dysrhythmia, valvular heart disease/endocarditis, recent MI, different between R+L BP |
| What scoring system is used for TIA? | ABCD2 - age (60+), BP (S>140, D>90), clinical fetaures (unilateral weakness (2), speech disturbance without weakness), duration (60+mins (2), 10-59mins ), diabetes - score from 0-7 |
| What is the function of exteroceptors? | Relay sensory information from outside world to CNS |
| What is the function of proprioceptors? | Relay information about posture and movement to the CNS |
| What is the function of interoceptors? | Raly information about the internal environment and organs to the CNS |
| What modality of information do the dorsal roots carry? | Sensory - posterior root - afferent |
| What modality of information do the ventral roots carry? | Motor - anterior root - efferent |
| What direction does an afferent neurone carry information? | Towards the CNS |
| What direction does an efferent neurone carry information? | Away from the CNS - exiting CNS |
| What type of sensory fibres are unmyelinated? | C fibres - group IV |
| What sensory receptors do A-alpha axons carry information from? | Proprioceptors of skeletal muscle - thickly myelinated - group I |
| What sensory receptors do A-beta axons carry information from? | Mechanoreceptors of skin - moderately myelinated - group II |
| What sensory receptors do A-delta axons carry information from? | Pain, temperature - thinly myelinated - group III |
| What type of receptors pick up vibration? | Pacinian corpuscle |
| What type of receptors pick up pressure? | Merkel disk receptor |
| What type of receptors pick up skin stretch? | Ruffini ending |
| What type of receptor picks up stroking and flutter? | Meissner corpuscle |
| Is the receptive field of pacinian corpuscles or Messner's corpuscles bigger? | Pacinian corpuscle receptive fields are much larger |
| What are the clinical features of intracerebral haemorrhage? | Bleeding into brain parenchyma - usually massive and fatal - occurs in chronic hypertension - headache, focal neurological deficit, decreased conscious level |
| What is the treatment of a intracerebral haemorrhage? | Control of hypertension is vital - urgent neurosurgical clot evacuation occasionally - antiplatelet and anticoagulant drugs are contraindicated |
| What are the clinical features of a cerebellar haemorrhage? | Headache, often followed by stupor/coma and nystagmus/ocular palsies etc - gaze deviates towards the haemorrhage - skew deviation with torticollis (head tiliting) - - acute hydrocephalus |
| What are the causes of subarachnoid haemorrhage? | Saccular (berry) aneurysms (70%): in circle of Willis, can be spontaneous rupture or pressure symptoms - arteriovenous malformation (10%): cause coal epilepsy, once ruptured has tendency to re-bleed - no lesion found in 15% |
| What are the clinical features of a subarachnoid haemorrhage? | Sudden, devastating thunderclap headache, often occipital - followed by vomiting, neck pain, Kernig's sign, photphobia, drowsiness, collapse - decreased conscious level, focal neurological deficit - papilloedema |
| What is the treatment of arteriovenous malformation? | Surgery, endovascular embolisation, stereotactic radiotherapy, conservative |
| What is Kernig's sign? | Thigh bent at the hip and knee at 90 degrees, subsequent extension of the knee is painful -> resistance |
| What investigations would you carry out in subarachnoid haemorrhage? | CT (may be negative though) - cerebral angiography is gold standard - LP not necessary if confirmed by CT, but is not then carry out: xanthocromic CSF |
| What are the complications of subarachnoid haemorrhage? | Obstructive hydrocephalus - arterial spasm (poor prognostic feature) - re-bleed - delayed ischaemic deficit, hyponatraemia - seizures |
| What is the management of subarachnoid haemorrhage? | Bed rest & supportive measures - contorl hypertension - dexamethasone to reduce cerebral oedema (also stabilises the BBB) - nimodipine reduces mortality - analgesia & anti-emetic - surgical clips/coils in selected |
| What are the clinical features of a subdural haemorrhage? | Usually follows head injury - interval between injury and symptoms can be days-months - chronic in elderly, with anticoagulants - headache, drowsiness, confusion, fluctuating consciousness - focal deficits - epilepsy - stupor, coma & coning |
| What feature will be seen on CT/MRI in subdural haemorrhage? | Clot ± midline shift - crescent shape |
| What is the treatment of a subdural haemorrhage? | Monitoring, less immediate attention - Irrigation/evacuation - burr twist drill/burr hole |
| What are the clinical features of a extradural haemorrhage? | Trauma to pterion - tearing of middle meningeal brach, skull vault fracture - head injury -> brief unconsciousness -> improvement (luccid level) -> stuporose, ipsilateral dilated pupil and contralateral hemiparesis with rapid transtentorial coning |
| What are the later features of a extradural haemorrhage? | Bilateral, fixed pupils, tetraplegia and respiratory arrest follow |
| What feature will be seen on CT of a extradural haemorrhage? | Lens shaped haematoma |
| What is the management of a extradural haemorrhage? | Immediate imaging (CT) - neurosurgery |
| Thunderclap headache? | Subarachnoid heamorrhage |
| Xanthrochromic lumbar puncture? | Subarachnoid haemorrhage |
| Luccid period after head trauma - often followed by sudden collapse or deterioration? | Extradural haemorrhage |
| Cogwheel rigidity? | Parkinson's - spasticity over rigidity |
| "Woody texture" muscle swelling? | Duchenne or Becker muscular dystrophy |
| Raised CK? | Muscular dystrophy |
| Toe walker or Gower's sign positive? | Muscular dystrophy |
| "Mask like" expression? | Parkinson's |
| "Fluctuating" cognitive deficit? | Delirium or Lewy body dementia |
| What diseases have REM disturbance? | Lewy body dementia or Parkinson's |
| Vivid visual hallucinations normally of children and not threatening? | Lewy body dementia |
| "acute onset" cognitive disturbance that fluctuates? | Delirium |
| Personality/behavioural changes and then dementia? | Frontotemporal dementia (Pick's disease) |
| Memory and personality problems in someone with a history of cardiovascular disease? | Vascular dementia |
| Stepwise deterioration in cognitive ability? | Vascular dementia |
| Pain on loud noise? | Facial nerve palsy |
| Cause of a painful third nerve palsy? | Aneurysm |
| Myalgia + myositis + myoglobulinaemia/urea? | Rhabdomyolysis (DIC and renal failure) |
| Inflammatory myopathy with poor response to steroids? | Inclusion body myositis? |
| Weakness + frontal balding + cataracts + ptosis? | Myotonic dystrophy (onset 30s, positive family history) |
| Leg symptoms + midline shift? | Falcine herniation |
| Back pain worse on coughing? | Slipped disc |
| Headache worse on coughing? | POsterior foss issue |
| Bilateral sciatica + male sexual dysfunction? | Cauda equina |
| What are the clinical features of cauda equina syndrome? | Severe back pain - saddle anaesthesia - bladder/bowel dysfunction - sciatica - paraplegia - absent ankle reflex - sexual dysfunction - gait disturbance |
| What does pleocytosis on CSF rule out? | Bacterial meningitis |
| What is migraine prophylaxis? | 1st line: proranolol, topiramate or amitriptyline| 2nd line: valproate, pizotifen, gabapentin, pregabalin |
| Injury to the upper brachial plexus? | Erb's palsy (waiter's tip) |
| Injury to the lower brachial plexus? | Klumpke's palsy (claw hand) |
| What injury is Simmonds test positive in? | Achilles tendon rupture |
| What is the nernst potential? | When the force of diffusion across the cell membrane = the electrical force attracting potassium into the cell |
| What is nociceptive pain? | Pain from injury, relayed through a normal nervous system |
| What is nueropathic pain? | Pain generated within the nervous system| "burning, shooting, tingling"| allodia (pain from stimulus that shouldn't cause pain) or hyperalgesia (more pain than expected)| amitriptyline, gabapentin, opioids, ketamin, capsaicin |
| What is the most important histopathological indicator of CNS injury? | Gliosis - astrocytes undergo hyperplasia and hypertrophy - nucleus enlarges and nucleolus becomes prominent |
| After what length of time of arterial supply to the brain being shut off does irreversible degeneration begin? | 4 minutes |
| Do neurons metabolise glucose through aerobic or anaerobic respiration? | Aerobic - can only do this - why brain receives proportionally so much more blood |
| What is a coup injury? | Injury directly at the point of impact - usually skull |
| What is a contracoup injury? | Injury diammetrically opposite the point of impact - usually skull |
| What is transcalvarium? | A swollen brain will herniate through any defect in the dura and skull - dilatation of pupil on same side as lesion |
| How does Botulinum toxin work? | Toxins cleave presynaptic proteins involved in vesicle formation and block vesicle docking with pre-synaptic membrane - rapid onset weakness without sensory loss |
| Complicated presentation of proximal and distal problems? | Plexopathy should be considered |
| What are the clinical Friedrich's ataxia? | Autosomal recessive - progressive damage to nervous system (spinal cord) - does not affect cognition - muscle weakness in arms and legs, loss of co-ordination, visual impairment, hearing impairment, slurred speech, scoliosis, pes cavus, diabetes |
| What the signs found in Friedrich's ataxia? | Cerebellar: nystagmus, dysarthria, dysmetria| LMN: absent deep tendon reflexes| pyramidal: extensor plantar responses, distal weakness are found| dorsal column: loss of vibratory and proprioceptive sensation occurs| cardiomegaly |
| What is the treatment of Friedrich's ataxia? | Surgical interventions (spinal screwing), goal is to keep patient mobile for as long as possible - physiotherapy |
| What reinforcement can be used when assessing deep tendon reflexes of the lower limbs? | Pulling interlocked fingers |
| What reinforcement can be used when assessing deep tendon reflexes of the upper limbs? | Teeth clenching |
| Dorsal column? | Fine touch, conscious proprioception and vibration - fibres cross in the medulla |
| Spinothalamic tract? | Pain, temperature, coarse touch and deep pressure - fibres cross segmentally (at spinal level) |
| Corticospinal tract? | Fine, precise movement, particularly of distal limb muscles (e.g. digits) - around 85% of fibres cross in the caudal medulla at the decussation of the pyramids, uncrossed fibres cross segmentally |
| Rubrospinal tract? | Excitatory control of limb flexor muscles - fibres originate in red nucleus of midbrain and then decussate at this level |
| Tectospinal tract? | Mediates reflex movement due to visual stimuli - fibres originate in the superior colliculus |
| Vestibulospinal tract? | Excitatory input to "antigravity" extensor muscles - fibres originate in the vestibular nuclei of the pons and medulla |
| Reticulospinal tract? | Many functions including the influence of voluntary movement - fibres originate in areas of the reticular formation in the pons and the medulla |
| Vestibulo-cerebellum? | Main function is maintaining balance - input from vestibular nuclei and projects to reticular formation and vestibular nuclei and from there to the spinal cord via reticulospinal and vestibulospinal tracts |
| Spinocerebellum? | Posture & muscle tone, control bum pressure & joints - input from spinocerebellar tracts carrying proprioception, touch & pressure information-projects to the thalamus, red nucleus & reticular formation to influence cortico-,rubro-&r eticulospinal outputs |
| Pontocerebellum? | Muscle coordination e.g. from playing the violin - input from pontine nuclei, which in turn receive fibres from the contralateral cerebral cortex - projects to the thalamic area (that in turn projects to the motor cortex) and to red nucleus |
| Pyramidal tracts? | Corticospinal |
| Causes of syncope? | Neurally mediated (reflex): vasovagal, situational, carotid sinus hypersensitivity, glossopharyngeal nueralgia - orthostatic hypotension - autonomic failure - cardiac arrhythmias - cardiopulmonary disease - cerebrovascular - psychogenic - substance abuse |
| Lower motor neurone lesion? | Wasting, fasciculation, decreased tone, decreased or absent reflexes, flexor plantars |
| Upper motor neurone lesion? | Increased tone, brisk reflexes, pyramidal/corticospinal pattern of weakness (=weak extensors in arm, weak flexors in the legs) |
| Purely fatigable motor symptoms? | Neuromusclar junction problem - myasthenia gravis |
| Shoulder abduction? | Deltoid - axillary nerve - C5 |
| Elbow extension? | - triceps - radial - C7 |
| Finger extension? | Extensor digitorum - post. interosseus - C7 |
| INdex finger abduction? | First dorsal interosseus - ulnar - T1 |
| Hip flexion? | Iliopsoas - femoral - L1/2 |
| Knee flexion? | Hamstrings - sciatic - S1 |
| Ankle dorsiflexion? | Peroneals - common peroneal and sciatic - L4/5 |
| Great toe dorsiflexion? | Extensor hallucis longus - common peroneal nerve - L5 |
| Ankle reflex? | S1/2 |
| Knee reflex? | L 3/4 |
| Biceps relfex? | C5/6 |
| Triceps reflex? | C7/8 |
| Glove and stocking sensory loss? | Length dependent neuropathy |
| Cerebellar signs/co-ordination? | Broad based and unsteady gait - intention tremor/ataxia (finger nose test and knee/heel test) - dysdiadochokinesis (clumsy fast alternating movements) - nystagmus and dysarthria |
| Extrapyramidal symptoms (Parkinsonism)? | Bradykinesia, rigidity, resting tremor, impaired gait and posture - hypomimia, hypophonia - reduced arm swing, stooped posture, small steps, festination, turning en bloc - impaired postural reflexes - assymetry in PD |
| Function of frontal lobe? | Generates novel strategies and has executive functions - enables self-critiscism and trying again - PFC has connections to other cortices: basal ganglia, limbic system, thalamus and hippocampus |
| Frontal lobe dysfunction? | Personality dysfunction, parapesis, paratonia, grasp reflex, frontal gait dysfunction, cortical hand, seizures, incontinence, visual field defects, expressive dysphasia, anosmia |
| Temporal lobe dysfunction? | Memory dysfunction (especially episodic), agnosia (visual and sensory modalities in particular), language disorders eceptive dysphasia, visual field defects, auditory dysfunction, limbic dysfunction, temporal lobe epilepsy |
| Parietal lobe dysfunction? | Visual field defect, sensory dysfunction (visual and sensory), dyspraxia, inattention, denial |
| Aggressive MS treatment? | Tysabri |
| Relapsing and remitting MS treatment? | Beta interferon and glatiramer acetate |
| Frequent presenting features of MS? | Visual compromise, stiffness and weakness |
Created by:
fmprentice