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217 Cards in this Set
- Front
- Back
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Features of Lambert Eaton syndrome
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increased muscle strength after repetitions
limb girdle weakness hyporeflexia Autonomic: dry mouth, impotence, difficulty micturating NOT a feature = ophthalmoplegia and ptosis |
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Pathophysiology of Lambert Eaton syndrome
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Ab directed against pre-synaptic voltage gated calcium channels in peripheral nervous system
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Classic triad of Wernicke's encephalopathy
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ataxia
confusion ophthalmoplegia nystagmus NOT confabulation (in Korsakoff's) |
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Features of Lewy body dementia
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visual hallucinations
progressive cognitive decline Parkinsonism sensitive to neuroleptics (haloperidol, chlorpromazine) |
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Physiology of neuroleptic malignant syndrome
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massive dopamine blockade
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Visual examination in craniopharyngioma
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bitemporal hemianopia, lower visual fields affected more significantly
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Visual examination in pituitary tumor
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bitemporal hemianopia, superior visual fields affected more significantly
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Features of parietal lobe lesions
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astereoagnosia (inability to tell things by touching them)
hemi-neglect apraxia sensory inattention inferior homonymous quadrantanopia Gerstmann's syndrome = L-R disorientation, alexia, acalculia, finger agnosia |
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Features of occiptal lobe lesions
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homonymous hemianopia
cortical blindness visual agnosia |
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Features of temporal lobe lesions
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Wernicke's aphasia
superior homonymous hemianopia auditory agnosia difficulty recognising faces (prosopagnosia) |
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Features of frontal lobe lesions
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Broca's (expressive) aphasia
disinhibition preservation anosmia inability to generate a list |
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Features of normal pressure hydrocephalus
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urinary incontinence
apraxia, gait abnormality (similar to Parkinson's) dementia |
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Features that point to diagnosis of motor neuron disease
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fasiculations
absence of sensory symptoms LMN signs in arms UMN signs in legs wasting of small hand muscles |
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T/F Nerve conduction studies are normal in motor neuron disease.
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True
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Features of neurofibromatosis type 1
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Cafe au lait spots
axilalry/groin freckles peripheral neurofibromas Lisch nodules scoliosis |
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Which chromosome is implicated in neurofibromatosis type 1?
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17 (think neurofibromatosis has 17 characters!)
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Features of neurofibromatosis type 2
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bilateral acoustic neuromas (vestibular schwannoma)
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Common side effect of metoclopramide
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extra-pyramidal symptoms
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Treatment of stroke
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rule out hemorrhage, then aspirin
if under 3 hours: thrombolysis with tPA/streotokinase |
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Features of cluster headache
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watery eyes
intense pain and redness around one eye nasal stuffiness pain occurs 1-2x per day ptosis and miosis |
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Features of Meniere's disease
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aural fullness
tinnitus hearing loss vertigo lasting min/hours |
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Features of BPPV
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vertigo for a few seconds/min
certain positions nystagmus |
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Managment of Meniere's disease
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draining
thiazides |
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Management of BPPV
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spontaneous recovery
Epley's and Brant-Daroff maneuveres surgery |
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Features of Von Hippel-Lindau disease
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cerebellar and retinal hemangiomas, vitreous hemorrhage
renal cysts adenomas phaeochromocytoma |
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Treatment for MS
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interferon beta
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Treatment of restless leg syndrome
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dopamine agonist, eg ropinirole
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Pharmacological treatment of Alzheimer's
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acetylchoine esterase inhibitors (donepezil) for mild-moderate
NMDAr antagonist (memantine) for moderate-severe |
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What runs through the cavernous sinus?
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CN 3, 4, 5 (V1 & 2, not mandibular), 6
internal carotid artery |
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SEs of levo-dopa
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postural hypotension
psychosis on-off effect arrhythmias dyskinesias N & V |
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What is a common infective cause of Guillian Barre syndomre
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Campylobacter jejuni
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what are the 4 patterns of MS
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Relapsing Remitting
Progressive relapsing Primary progressive Scondary progressive (initially relapsing then progresses to progresive) |
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Which HLA is associated with MS
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HLA-DR2
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What is the aetiology of MS
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Genetic - HLA-DR2
Environmental - MS is more common in regions with less sun exposure and less vit D (retain risk of area in which you grew up < 15) Association with EBV |
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What questions do you want to ask in a history of MS?
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Onset
Initial neurological deficit Any episodes of spastic paraparesis, hemiparesis or tetraparesis; limb paraesthesiae; reversible visual loss or ocular pain, loss of central visual field (optic neuritis) weakness, incoordination, band sensations around trunk and limbs; lancinating pain, speech impairment, sphincter disturbances, sensory loss, vertigo, gait difficult Lhermitte's phenomenon (electric shock-like pain radiating down the spine, triggered by neck flexion) Precipitating factors: heat; infection, fever, pregnancy, exercise Disease pattern and temporal profile Complications associated with neurological deficit (aspiration pneumonia, UTI, mechanical injuries, limb contractures, pressure areas and painful mm spasms) Functional level of patient, social and occupational difficulties associated with sexual function Mood Fatigue Family history, patient's place of birth Pregnancy - 20-30% increase in relapse rate first month after delivery Different treatments and adverse effects |
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Examination of patient with MS
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Full neurological exam
part. visual examination - ecternal ocular movements, INO, optic atrophy, afferent pupillary defect Spinal cord signs bulbar signs cerebellar signs cerebral hemisphere signs MMSE - can lead to cognitive impairment |
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What is internuclear opthalmaplegia
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Disease of conjugate lateral gaze
Weakness of adduction in one eye as a result of damage to the ipsilateral medial longitudinal fasciculus. There is nystagmus in the abducting eye. When affected eye tries to look contralaterally it cannot adduct Often bilateral in MS |
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What are the different MS variants?
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Delvis = neuromyelitis optica = episode of optic neuritis and transverse myelitis occuring within a few weeks of one another
Benign MS: RR without major disability for 10 years Clinical isolated syndrome = single MS episode |
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Typical locations of MS plaques on MRI
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periventricular, corpus callosum, cerebellar peduncles, brainstem, juxt cortical region, dorslateral spinal cord
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What are dawson's fingers
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periventricular lesions extending superiorly into corpus callosum
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What investigations are done in MS
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MRI
T2 weighted - hyperintense lesions gadolinium shows up acute lesions CSF oligoclonal bands - antibodies depicted as bands on agragose gel Evoked potentials (visual/auditory/somatosensory) - generated by peripheral stimulation of a sensory organ |
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Features of MS on MRI
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a) Classical lesions perpendicular to ventricles and in corpus callosum—'Dawson's fingers'
b) Lesions tend to be periventricular, whereas in vasculitis they are more peripheral c) Subcortical U fibres, characteristic of multiple sclerosis d) Cerebellar (infratentorial) plaque e) Cortex may show atrophy |
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Differential diagnosis of MS
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SLE
HIV Sarcoidosis Spinal or brainstem lesion Metabolic disorder - Vit B12 deficiency Coag disorder |
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Management of MS
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Acute relapses - steroids
Underlying disease - Immune modulators: Interferon beta SE: depression, flu like; skin re; LFTs, platelet and WCC reduction; thyroid antibodies; can develop neutralising antibodes (reduce effectiveness of drug); glatiramer acetate; atalizumab Immunosuppressants: Methotrexate; Azathioprine |
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What is the definition of epilepsy?
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Chronic condition characterised by 2 or more unprovoked seizures
Seizure = transient neurological dysfunction caused by excessive activity of cortical neurons, resulting in paroxysmal alteration of behaviour and/or EEG changes |
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What are the risk factors for epilepsy?
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Family history
Head injury Meningitis/encephalitis MS Drugs (alcohol, heroin, MJ) Complex febrile convulsions Alzheimer's CVD |
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What is the difference between simple and complex seizures?
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Simple - no LOC
Complex - LOC (alteration of mood, memory, perception) |
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Do you get LOC in generalised seizures?
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Yes
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What are automatism and when do you see them?
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Brief unconcious behaviours
Chewing, swallowing, lip-smacking, scracthcing, fubling, running, disrobing, prior to LOC followed by distant staring unresponsiveness |
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What are the different types of generalised seizures that you can get?
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Tonic-clonic (grand mal):
Absence Tonic Clonic Myoclonic Atonic |
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Describe the features of a tonic clonic seizure
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Prodrome: unease or irritability hours to days before the attack (aura sometimes)
Tonic: tonic mm contractions, arm flexion and adduction, leg extension, 'cry' as respiratory mm spasm and air is expelled; 10-30 secs Clonic: clonus involving violent jerks of face and limbns, tongue biting, incontinence; < 90 secs Ictal autonomic outpouring (hypertension, tachycardia, hypersalivation, pupilary dilation) |
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Describe the symptoms felt after a tonic clonic seizure
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decreased LOC, flaccid limb and jaw, extensor plantar reflexes, loss of corneal reflexes
headache, confusion, aching mm, sore tongue, amnesia, elevated serum CK lasting hours |
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What are the features of an absence seizure?
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Non convulsive event - unresponsive for 5-10 seconds with arrest of activity, starring, blinking or eye rolling
No memory of event No postural loss b/e seizure doesn't spread across both hemispheres Ca is involved Generaly age of onset 6-7 girls> boys Remission in 80% by adolescence 20% turn into generalised tonic-clonic seizures |
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Features of a myoclonic seizure
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brief contractions localised to mm groups of one or more extremities or more generalised
age of onset 12-16 years generally seen in the am very responsive to therapy |
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What are the features of an atonic seizure
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loss of postural tone leading to drop attack
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What type of features are characteristic of partial seizures
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Simple vs complex
motor sensory autonomic psychiatric |
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What is a Jacksonian March?
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Symptoms of a seizure start in one location and spread to another
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What type of epilepsy is suggested by an aura of fear, olfactory or gustatory hallucinations, visveral or deja vu sensations?
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Temporal lobe epilepsy
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What type of seizures are suggested by contralateral focal sensory or motor phenomena
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Frontoparietal cortex seizures
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What can complex partial seizures sometimes resemble?
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schizophrenia or psychotic depression
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What is a non-epileptic (pseudo) seizure?
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Physical manifestation of a psychological disturbance
Normal EEG Paroxysmal episodes either organic (TIA, syncope, migraine) or psychogenic Rare to have physical injury, incontinence Usually occur during the day with other people present Features include: opisthotonos, rigidity, forced eye closure, irregular exctremity movements, shaking head, pelvic thrust, crying |
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Outline the common causes of seizures in infancy and early childhood
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Febrile
Congenital Inborn errors of metabolism perinatal injury |
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Outline the common causes of seizures in older adults
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Cerebral tumours
Neurodegenerative disease CVD |
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Outline the common cause of seizures in adolescents
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head injury
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What is Todd's post-ictal phenomena?
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Post-ictal depressed function of the local cortex involved producing focal weakness --> Todd's hemiparesis
Usually seen if seizures are prolonged or recurrent |
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When should a patient having a seizure be transferred to hospital?
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Status epilepticus or multiple seizures
First seizure Pregnancy or diabetic or injury |
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What questions should you be thinking about in the management of a first seizure?
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Was it actually a seizure?
LOC? What type? Any secondary injury (i.e. bitten tongue) Evidence of CNS dysfunction Precipitating factors Investigations to be ordered Should you start an anti-epileptic drug? |
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What causes seizures?
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In patient with known epilepsy
Hypoglycaemia ETOH excess of withdrawal Intercurrent infection Stress INadequate anticonvulsant therapy head injury In non-epileptic CNS (head injury, brain tumour, CVD, infection, hypertensive encephalopathy, Endocrine (hypoglycaemia, hyponatraemia, hypocalcaemia, hypomagnesia, uraemia) Systemic disorder (eclampsia, hypoxia, hypotension, sepsis from renal tract, respiratory or skin infection) Drug related toxicity and withdrawal (TCAs, cocaine, tramadol, pethidine) |
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What are the major threats to life involved with seizures?
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Hypoxia
aspiration hyperthermia Cerebral oedema (if they last > 1 hour) |
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Immediate management of seizures in hospital?
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ABC
Lateral position O2 mask If seizure doesn't stop may want to give midazalam or diazepam Once seizure has stopped immediately follow with phenytoin to prevent recurrence |
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What investigations should be performed in new onset seizure?
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Bloods (FBC, EUC, LFTs, BHCG, CMP, serum glucose, anti convulsant levels)
NB: vigorous seizure alone can cause hyperkalaemia and acidosis CT head LP if suspsect SAH or infection EEG |
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What is the mechanism of action of phenytoin?
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Na channel blocker
Limits the firing frequency of neurons |
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MOA of Carbemazapine
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Na channel blocker (limits the firing frequency of neurons)
Enhances GABA Activates adenosine receptors which limits the release of excitatory transmitters from the presynaptic terminal e.g., glutamate |
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MOA sodium valproate
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Decreased metabolism of GABA (enhances GABA inhibition)
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Trade names for
Phenytoin Carbemazapine Sodium valproate |
Phenytoin = dilantin
Carbemazapine = tegretol Sodium valproate = epilim |
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Which anti-epileptic cannot be used in pregnancy
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sodium valproate
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Which anticonvulsants are used for generalised epilepsy?
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sodium valproate
carbemazapine |
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Which is the drug of choice for partial epilepsies
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Carbemazaepine
IF it fails can use sodium valproate or phenytoin |
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MOA phenobarbitone
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Barbituate (increases Time that GABA channels stay open for
+ decreases release of glutamate from the presynaptic terminal |
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Which anticonvulsants are used in absence seizures?
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Ethosuximide
Sodium valproate |
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Mechanism of action of ethosuzimide
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INcreases seizure threshold
Suppresses characteristic spike and wave pattern in absence seizures |
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What is status epilepticus?
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Seizure that lasts for > 30 mins without spontaneous cessation or recurrent seizures > 30 mins without full return to consciousness inter-ictally (i.e. regaining consciousness in between)
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Management of status epilepticus
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Protect the airway, always check glucose
Termination of seizure activity Clonazepam OR diazepam OR midazalam These are short acting so must follow these with Phenytoin or sodium valproate Follow this with ongoing antiepileptic therapy |
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What questions should be asked to distinguish syncope from a seizure
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Time of onset
Precipitating factors Position Onset - sudden or gradual LOC Ura Colour Autonomic effects e.g., diaphoresis (common in syncope) Duration Incontinence Post-ictal confusion Injury Automatisms |
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What do slow background EEG frequencies in the inter-ictal period suggest?
Normal background EEG frequencies |
SLow background - underlying insult
NOrmal - primary epilepsy |
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What is the prognosis of patients with epilepsy?
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70% good seizure control and achieve remission
20% need regular medication and may have breakthrough seizures 5-10% poorly controlled |
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which tumours is located at the cerebellopontine angle?
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vesticular schwannoma "acoustic neuroma"
makes up 80-90% of tumours of the CPA |
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How do patients with vestibular schawnnoma's present?
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progressive unilateral or asymmetrical sensorineural hearing loss
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Where does the vestibular schwannoma originate from?
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CNVIII in internal auditory canal, expanding into bony canal and cerebello-pontine angle
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What do bilateral vestibular schwannoma's suggest?
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neurofibromatosis type 2
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are vestibular schwannoma's benign or malignant?
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benign
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What clinical features do vestibular schwannoma's have?
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CNVIII - hearing loss, tinnitus, dysequilibrium, difficulty walking
V: decreased temperature sensation and face paraesthesias VII: facial nerve palsy N+V Ataxia and raised ICP are late features |
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How do you manage vestibular schwannoma's?
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stereotacic radiosurgery = treatment of choice
surgery if > 3cm, brainstem compression, edema, hydrocephalus |
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RF for vestibaular schwannoma's?
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neurofibromatosis type 2
exposure to loud noice childhood exposure to low dose radiation parathyroid adenoma |
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How can pituitary adenomas present?
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Mass effects: headache, bitemporal hemianopis, CN III, IV< V1, V2, VI palsy
endocrine effects: can be functional or non-functional Pituitary apoplexy = sudden expansion of mass due to haemorrhage or necrosis - abrupt onset HA, visual disturbances, ophthalmoplegia, reduced mental status, panhypopituitarism CSF rhinorrhea and seizures signs and symptoms of SAH (rare) |
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In what order will a compressive pituiary adenoma ffect the endocrine hormones that is secretes?
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"Go Look For The Adenoma Please"
GH LH FSH TSH ACTH Prolactin |
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How does hyperprolactinaemia
present? |
infertility
amenorrhea galactorrhea decreased libido |
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What are the DDx if you spot a ring enhancing lesion on CT with contrast?
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Most common causes =
mets abscess glioblastoma |
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How might a tumour in the cerebral hemisphere present?
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Raised ICP
Progressive neurological deficits specific to site of lesion (usually subacute onset) Frontal: personality change, apathy, impaired intellect Parietal: contralateral homonymous hemianopia, cortical sensory loss and motor deficit Seizures - typically focal |
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HOw might a cerebellar tumour present?
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ataxia ipsilateral to lesion
vertigo, N/V impaired articular of speech, respiratory movements, motor learning |
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What is the most common brain tumour seen clinically? Mets or primary?
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Mets
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what are the most common sites making cerebral mets?
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lungs, breast
can also be kidney, colorectal, thyroid, stomach, prostate, testis, melanoma |
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What is the ideal imaging study used for brain mets?
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contrast enhanced MRI
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What radiologic features can differentiate brain mets from other CNS lesions?
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multiple lesions
localisation at the junction of grey and white matter circumscribed margins large amounts of vasogenic oedema compared to the size of the lesion usually ring enhancing |
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what is the prognosis of someone with brain mets?
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median survival without treatment once symptomatic is 1 month, with optimal treatment 6-9 months but varies depending on primary
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What is the most common primary intra-axial brain tumour?
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astrocytoma
4 grades including low grade/diffuse and glioblastoma multiforme |
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Where is the most common place to find an astrocytoma?
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cerebral hemipsheres
then cerebellum, brainstem, spinal cord |
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Treatment options for astrocytomas?
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surgical resection (usually too large)
radiation chemo if tumour progression |
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Are meningioma's benign or malignant?
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Mostly benign (1% malignant)
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What cell type do meningioma's arise from
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arachnoid cells
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What features do mengiomas usually present with?
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majority are asymptomatic
if over hemispheres can present with seizures, progressive hemiparesis If at skull base can present with cranial neuropathies |
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Which brain tumours are contrast enhancing?
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Meningioma
Glioblastoma multiforme Mets Vestibular schwannoma oligodendrogiloma show some contrast enhancement |
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Which brain tumours are not contrast enhancing?
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astrocytoma
oligodendroglioma - some show contrast enhancement |
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Treatment of meningioma?
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surgery = treatment of choice if symptomatic or progression on sequential imaging
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Which brain tumours have the best survival rate?
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meningiomas (mostly benign)
Oligodendroglimoa - medial surval 16 years - most eventually progress to malignancy |
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Which brain tumour often causes hyperostosis of adjacent bone, often calcified
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Meningioma
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What symptom/s occur with distortion of the upper brainstem cause?
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Decreased level of consciousness
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What symptoms occur with compression of the medulla (e.g. when cerebellar tonsils herniate caudally through the foreamen magnum)
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impaired consciousness, respiratory depression, bradycardia, decerebrate posturing and death.
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Treatment for pituitary apoplexy?
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corticosteroids STAT
+/- surgical decompression |
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Treatment for prolactinoma?
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Dopamine agonists (bromocriptine)
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Treatment for acromegaly
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somatostatin analogue (octreotide) +/- bromocriptine
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What drug inhibits cortisol production?
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ketaconazole
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What is the most common location for carotid artery stenosis
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Near the common carotid bifurcation into internal and external carotids
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How may carotid artery stenosis present?
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TIA or stroke OR
Retinal insufficiency or infarct due to emboli occluding central retinal artery or branches permamently or temporarily (amaurosis fugax) MCA occlusive symptoms |
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At what level of occulsion does carotid artery stenosis require an endarterectomy or stenting
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> 70% stenosis and symptomatic
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What investigations should be done in someone with carotid artery stenosis
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FBC, coags
Fundoscopy (cholesterol emboli in retinal vessels = HOllenhorst plaques) carotid duplex doppler US - size of lumen and flow velocity - least accurate Angiogram = gold standard but high risk of stroke 1/200 MRA: safter than angiogram but may overestimate stenosis |
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Pathophysiology of TIAs
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Emboli or
In situ thrombosis of an intracranial vessel |
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What are we worried about in someone whose just had a TIA?
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It is an independent RF for a stroke within the next 7 days
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What are the 3 causes of ischaemic infarct
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Arteriogenic emobolisation
Cardiogenic embolisation Large vessel thrombus |
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What is a lacunar infarct?
Which areas do they occur |
Occlusion of a small artery branching off from the MCA into deep grey and white matter
Usually in the basal ganglia, thalamus, posterior limb internal capsule |
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What are some features of a lacunar infarct?
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Pure motor hemiparesis: contralateral arm, leg, face
pure sensory loss: hemisensory loss (usually thalamic) ataxix hemiparesis: ipsilateral ataxia and leg paresis dysarthria-clumsy hand syndrome: dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness |
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Risk factors for a lacunar infarct
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age
HTN |
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Most common causes of intracerebral haemorrhage
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HTN
Trauma Bleeding diatheses Amyloid angiopathy Vascular malformations Drugs (cocaine and amphetamines) Tumours |
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What are the mechanisms of brain injury in ICH
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Mechanical injury secondary to expanding clot
Raised intracranial pressure Herniation secondary to raised ICP |
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What is the different in Sx between haemorrhage and SAH, ischaemic stroke
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Haemorrhage - the sx begin gradually and form over a few hours, they do not begin abruptly and are not maximal at onset
cf. ischaemic and SAH |
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Apart from Sx related to the location of the ICH what other features can they have?
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Headache - traction on meningeal pain fibres or blood in CSF
Seizures Stupor/coma - if stupor is due to involvement of reticulating activating system then may have good recovery otherwise this is an ominous sign |
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What is the main cause of SAH?
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Trauma (most common)
Rupture of arterial aneurysms (75-80%) idiopathic (14-22%) AVMs (5%) coagulopathies, vasculitidies, tumours |
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What is the classic symptom of SAH
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Sudden severe headache - worst headache of my life
May get brief LOC (raised ICP, ischaemia, seizure) N/V, photophobia Meningismus - neck pain/stiffness, positive kernigs sign Usually no focal neurologic signs unless bleeding occurs into the brain and CSF at the same time but may get CN palsy, hemiparesis Occular haemorrhage due to sudden raised ICP compressing central retinal vein Reactive HTN |
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Differential diagnosis of severe sudden onset headache
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SAH
Sentinel bleed dissection/thrombosis of aneurysm Venous sinue thrombosis benign exertional headache |
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What is a sentinel bleed
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SAH like symptoms lasting < 1 day (thunderclap HA)
May have blood on CT or LP 50% of patients with full blown SAH give history suggestive of sentinel blled within past 3 weeks |
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Risk factors for SAH
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HTN
Pregnancy/parturition in patients with pre-existing AVMs, eclampsia OCP Substance abuse (smoking, cocaine) Conditions associated with high incidence of aneurysms (e.g., polycystic kidney disease, fibromuscular dysplasia, connective tissue disease) |
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Investigations for suspected SAH?
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FCB, coags
Non contrast CT - NB may be negative if small bleed or presentation delayed several days CTA/MRA/cerebral angiography (gold standard) - localisation and treatment planning If CT -ve do LP for xanthocrhomia (yellow appearance of CSF to indicate presence of RBCs) LP opening pressure > 18mmH2O |
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What is cerebral perfusion pressure
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MAP - ICP
MAP = DP + 1/3 (SBP-DBP) |
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Outline the immediate and early medical/surgical management of a patient with SAH
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1. Coagulation problem
Coag screen if abnormal consider FFP and/or Vit K if PT or aPTT > 1.3; If warfarin or antiplatelet cease 2. DVT prophylaxis - TED stockings - no heparin or clexane 3.BP if S< 160 D < 100 - no BP lowering, monitor half hourly if S > 160 D > 100 on 2 separate recordings 5 mins apart - clonidine or hydralazine 4. Neurosurgical management if aneurysm - clip or coil - decreases risk of early and late recurrences 5. Stool softeners, bedrest, anaglesia |
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Complications with SAH
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Vasospasm
hydrocephalus neurogenic pulmonary oedema hyponatraemia DI arrhythmias |
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What is vasospasm
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constriction of blood vessels in response to arterial blood clot outside of vessels at the base of the brain
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When is the usual onset of vasospasm?
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4-14 days after SAH
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Symptoms of vasospasm
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LOC
focal deficit (speech or motor) confusion |
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What is the triple therapy for vasospasm
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Hypertension
Hypervolaemia Haemodilution |
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Risk factors for vasospasm
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smoking
increased age prior HTN large amount of blood on CT |
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Why do you get hydrocephalus with SAH
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blood obstructs CSF drainage or subarachnoid space
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What is the classic site of hypertensive haemorrhages
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basal ganglia
you can also get them in the putamen, thalamus, cerebellum and pons |
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Clinical features of infarction of ACA
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Primarily foot and leg involvement (motor and sensory)
Incontinence (loss of bladder control - hypertonic detrusor) grasp reflex |
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Clinical features of middle cerebral artery
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Hemiparesis and sensory (contralateral)
homonomyous hemianopia (optic radiation) If dominant hemisphere - aphasia, Gerstmann syndrome in parietal (agraphia, acalculia, R/T finger agnosia) Non-dominant - contralateral neglect, dressing and construction apraxia |
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Clinical features of infarction of lenticulostriate arteries
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pure motor hemiparesis and hemisensory deficit
Ataxia +/- dysarthria |
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Clinical features of infarction of basilar artery
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quadriplegia and death unless there are good anterior collaterals
generalised weakness, gait difficulty, decreased responsiveness progressing to coma. dysarthria, shivering, blurred vision |
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Clinical features of occlusion of PCA
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homonymous hemianopia
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Features of PICA infarction i.e. lateral medullary syndrome
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ipsilateral ataxia
ipsilateral horners ipsilateral facial sensory loss contralateral impairment of pain and temp nystagmus vertigo N?V dysphagia and dysarthria NO MOTOR HEMIPARESIS |
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What is the pattern of LP results for fungal infections and TB
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increased protein
Decreased glucose Increeased lymphocytes |
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which thumb mm does the median nerve supply?
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opponens policis brevis
flexor pollicis brevis |
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What nerve supplies thumb adduction?
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ulnar nerve
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How does someone with a lacunar infarct present?
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Basal ganglia, thalamus, posterior limb internal capsule
Pure motor hemiparesis: contralaeteral arm, leg, and face Pure sensory loss: hemisensory loss (usually thalamic) ataxix hemiparesis: ipsilateral ataxia and leg paresis Dysarthria-clumsy hand syndrome (dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness) |
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Occlusion of which artery usually leads to locked in syndrome?
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proximal basilar artery
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Where is the lesion if you have loss of pain and temperature on the right side of the boyd and the left side of the face?
which artery is affected? |
left medulla
lateral medulla or wallenburg syndrome PICA |
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What is the hallmark sympom of vertebro basilar insufificneyc
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vertigo
Cna also have nystagmus, limb ataxia, truncal ataxia, contralateral pain and temp, CN - visual field defects Hemi-or quadriplegia |
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Signs of upper motor neuron lesion
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weakness
hyperreflexia increased tone up-going Babinksi **refelxes and tonicity may develop over days/weeks and may look like LMN in the beginning |
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Signs of lower motor neuron lesion
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weakness
atrophy fasiculations hyporeflexia hypotonia ABSENT Babinksi |
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Where is the lesion?... in one sided face, arm, leg weakness/paralysis WITHOUT sensory features
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must be above medulla and below cortex
most common site = contralateral internal capsule supplied by MCA/lentriculostriate system |
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What is a lacunar infarct?
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Lacunar infarcts are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%). They occur less commonly in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum.
usually only motor is affected! |
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Where is the lesion?... in one sided face, arm, leg, weakness/paralysis WITH sensory, oculomotor, visual, higher cortical deficits
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infarct of precentral motor strip w involvement of sensory neurons across the central sulcus
large territory MCA stroke, could be involving internal capsule |
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Where is the lesion...??
one sided arm and leg weakness/paralysis |
face is spared - lesion must be below foramen magnum
two areas: 1. contralateral arm and leg regions of primary motor strip - more likely if acute 2. ipsilateral (below pyramidal decussation) corticospinal tract from caudal medula (after corticobulbal tracts have departed) and above C5 - more likely if gradual, could be neoplasm |
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if the face is spared, where must the lesion be in a TIA/stroke?
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below the foramen magnum
because most of the CN efferents and the corticobulbar system remain largely above the foramen magnum |
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Where is a watershed infarct most likely?
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between territories of anterior and middle cerebral arteries
gives rise to proximal mm weakness - man in a barrel syndrome |
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Where is the lesion...??
One-sided arm and face weakness/paralysis |
precentral motor cortex (face and hands are side by side on the homonculus)
usually associated with Broca's aphasia if in dominant sphere, hemi-neglect in non-dominant most common cause = MCA (superior division) |
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Where is the lesion..??
One-sided arm weakness/paralysis |
can be:
1. peripheral nerve lesion - check for LMN signs... but would most likely have sensory signs too, CANNOT have pure motor loss unless lesion is just in anterior horn 2. discrete infarct affecting just contralateral are of precentral motor cortex - will have UMN signs |
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Where is the lesion...?
one sided leg weakness/paralysis |
could be:
1. leg region of precentral motor cortex - infarct of anterior cerebral artery 2. CsT below T1 (bc no arm weakness) - compression by tumor or MS 3. peripheral nerves supplying leg - injury or diabetes, but would probably have sensory loss too |
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Where is the lesion...??
Unilateral facial weakness/paralysis |
Bell's palsy - CNVII, usually 2ary to Herpes Zoster
could also be contralateral precentral motor strip, but would probably have arm and leg involvement if UMN lesion --> forehead and eyes will be spared |
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Where is the lesion...??
Bilateral arm weakness/paralysis |
bilateral medial portions of CsT aka central cord syndrome caused by syringomyelia or myelitis
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Where is the lesion..??
Bilateral leg weakness/paralysis |
could be:
1. parasagittal meningioma 2. bilateral infarct of anterior cerebral artery 3. CsT below T1 - may also present with cauda equina syndrome, which would involve sensory loss 4. neuromuscular disorders (GBS, lambert eaton, diabetic) - usually affects proximal mm |
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Where is the lesion...??
bilateral arm and leg weakness/paralysis |
could be:
1. bilateral motor strip 2. CsT after leaving foramen magnum but before reaching C5 3. cord transection above C5 - would have UMN signs, sphincter dysfunction, autonomic dysfunction |
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What are the lab values in Duchenne's muscular dystrophy? (CK, nerve conduction, EMG)
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CK: elevated, goes down in terminal stages of disease
nerve conduction: normal EMG: grossly abnormal |
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Definitive diagnostic test in Duchenne's muscular dystrophy
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immunohistochemical staining of mm biopsy --> absent dystrophin molecule
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Rx of dermatomyositis and polymyositis
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kids: almost always respond to steroids
adults: often require immunosuppressive therapy with azathioprine + corticosteroids |
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What is Wilson's disease and what is the Rx?
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excessive copper deposition --> degeneration of liver and basal ganglia --> dystonia, dysarthria, rigidity, tremor, chorea, psych
serum copper high, ceruloplasmin low Rx: copper-chelating agent (penicillamine) |
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Difference between Parkinsons's and multisystem atrophy
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MSA is usually symmetrical, absence of resting tremor, and little response to dopaminergic agents
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Rx of acute angle closure glaucoma
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reduce IOP --> acetazolamide or laser peripheral iridotomy
also, alpha agonists, cholinergic agents (pilocarpine), beta blockers, prostaglandins |
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What is cabergoline and what are its SEs?
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Dopamine receptor agonist
SEs: pulmonary, retroperitoneal, and cardiac fibrosis (same for all dopamine receptor agonists! bromocriptine, ropinirole, apomorphine) |
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Signs of acute angle closure glaucoma
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headache, painful and red eye, seeing halos, N&V, reduced VA
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CSF values in bacterial and viral meningitis
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Bacterial: cloudy, low glucose (<1/2 plasma), high protein, WCC 10-5000 polymorphs
Viral: clear/cloudy, normal glucose*, normal/raised protein, WCC 15-1000 lymphocytes Mumps and herpes encephalitis can be associated with low glucose level |
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Are reflexes normal in polymyositis?
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yes
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Middle cerebral artery stroke symptoms
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1. contralateral face-arm-trunk motor & sensory deficit
2. Broca's (superior branch) or Wernicke's (inferior) aphasia OR neglect if lesion in non dominant hemisphere 3. homonymous hemianopia 4. gaze preference toward side of lesion |
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Anterior cerebral artery stroke symptoms
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1. contralateral hemiparesis and sensory loss in leg
2. frontal lobe dysfunction |
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Posterior cerebral artery stroke symptoms
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1. homonymous hemianopia
2. if affects corpus callosum --> alexia |
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Lenticulostriate artery stroke symptoms
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1. pure motor or sensory hemiparesis
2. ataxic clumsy hand +/- dysarthria |
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Does small vessel disease have a greater effect on whtie matter or grey?
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white matter
More capillaries in grey matter - high metabolic demand - therefore if you interupt a few small vessels in grey matter won't get infarction - enough to ensure survival |
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How often does focal ischaemia in brain produce unconcsioussness?
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very rarely
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What is transient globlal amnesia?
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unable to lay down new memories
migraine equivalent that produces spasm in basilar artery or in distal territory - iscahemia of mesotemporal lobe that disables both hippocampi New goes onto stroke - a couple of hours where they can't lay down memories |
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Do you see neglect in dominant hemisphere strokes?
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not very often
Only if it is a very large stroke Otherwise usually just see neglect in non-dominant MCA strokes |
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What features will you have in a non dominant hemisphere MCA stroke? cf dominant?
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contralateral neglect
navigational difficulty dressing apraxia constructional apraxia Dominant aphasia Gerstmann syndrome, agraphia, acalculia, R/L confusion, finger agnosia |
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Do you get a visual field defect with ACA?
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NO
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Which artery supplies the macula?
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distal MCA
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If you get bilateral infarctions of PCA what do you present with?
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bilateral hemianiopa with cortical blindess
associated memory disturbance |
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Emoblus lodges at top of basilar?
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cortical blindness and often quadriparesis (damaged blood supply to cerebral peduncles - containing outflow from internal capsule)
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Which group is basilar occulsion common in?
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elderly
tortuous vessels Often present with slow progression to coma |
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How do small vessel infarcts present?
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Each is own syndrome - features may not occur toegether
pure hemiparesis - no sensory deficit or aphasia etc ataxic clumsy hand both of the above can occur in internal capsule and somewhere in pons clumsy hand + dysarthria pure hemi sensory deficit |
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what is the significance of transient hemiparesis?
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medical emergency
signals impending stroke |
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What heralds the onset of an uncal herniation?
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unialtaeral 3rd nerve palsy
contralateral weakness - compressing cerebrellar peduncles Uncus is area of temporal lobe right near medulla |
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What causes apneustic respiration?
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= prolonged pauses in respiration
caused by pontine lesion |
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What causes ataxic respiration
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= irregular respiration
medullary lesion poor prognosis |
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What can cause pin point pupils?
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opiate overdose
pontine lesion |
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Which direction are the eyes deviated towards in a supratentorial lesion?
pontine lesion? |
Supratentorial lesion - towards lesion - centre on that side has been destroyed, contralateral centre pushes eyes to side of lesion
Pontine lesion - away from lesion - horizontal gaze centre lateral aspect of pons - moves eyes to same side if destroyed moves eyes away |
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What is the oculocephalic reflex
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moves head - eyes will stay fixed or move away from side that you're moving head to
decreased OC - eyes will move with head = dolls eye movement - eyes are not being moved as they should be by vestibular system |
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What is the oculovestibular reflex?
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squirt hot and cold water into ear drum
cold water - eyes move to side of lesion hot water - move away from side of lesion Vestibular lesion - this is lost |
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Where is the lsion in decererbate rigidy?
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midbrain lesion
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Where is the lesion with decorticate posturing?
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corticospinal damage
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how long do brain reflexes need to be absent before you can pronounce brain death?
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24 hours
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Which tests can you do to determine brain death?
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ALL must be absent for 24 hours
pupils fixed and dilated caloric reflexes absent corneal reflexes absent no reflex to noxious stimuli gag reflex absent NO spontaneous respiration patients must not be on any sedative agents exclude reversible causes |
