Neuro Flashcards
WHat causes lateral medullary syndrome? What is this supplied by
Infarction of the lateral portion of the medulla oblingata
Posterior inferior cerebellar artery or vertebral artery
Features of lateral medullar syndrome
Loss of pain and temp sensation on the contralateral side of the body and on the ipsilateral side of the face (dysphagia, vertigo, dysarthria, horners syndrome and nystagmus)
Definition of parkinsonism
Collective term for a clinical syndrome that includes bradykineasia alongisde one other of
- tremor
- rigidity
- gait disturbance
Causes of parkinsonism
PD
Drug induced
Cerebrovascular disease
Dementia with lewy bodies
MSA
Progressive supranuclear palsy
Pathology of PD
Chronic progressive neurodegenerative disease linked to decreased dopamine production in the substrantia nigra
What gait is seen in PD
Shuffling
Diagnosis of PD
Mainly clinical
MRI
SPECT
What are parkinsons plus syndromes
A group of neurodegenerative diseases that consit of cardinal features of PD, alongside additional symptoms which include a reduced response to levodopa, dysarthria, autonomic dysfunction and supranuclear gaze palsy
Examples of the parkinsons plus syndromes
Multiple system dystrophy
Dementia with lewy odies
Progressive supranuclear palsy
Corticobasal degeneration
MEdications that are known to cause parkinsonism
Antipsychotics
metoclopramide
prochloperazine
tetrabenazine
sodium valproate
lithium
Signs and symptoms more consistent to the diagnosis of PD
Unilateral onset and patient asymmetry
Resting tremor
good response to levodopa
Levodopa induced dyskinea
Long disease course >10 yrs
Treatment of PD
- Levodopa or co-carledopa
- pramipexole or ropinorole
What drug can you use to improve dyskinesia affects of anti-parkinson medications?
Amantadine
What is the triad of NPH
Gait disturbance
Memory loss
Urinary Incontinence
Symptoms of L5/S1 disc prolapse
Low back pain
Sciatica
Limited straight leg raisiing
Loss of ankle reflex
Weakness of plantar flexion
Sensory loss in affected dermatome
A young otherwise healthy person who suddenly develops a stroke is likely to be caused by what?
Paradoxical embolus
Due to a patent foramen ovale
Imaging of choice if you were suspecting a paradoxical emboli secondary to patent FO
transoesophageal ECHO with doppler colour imaging
What is a common S/E of levodopa Tx
Dark urine
What is found in the CSF of patients with MS
Unpaired oligoclonal bands
S/E of topiramate
Weight loss
Renal stones
Congitive/behavioural changes
What is neuroepileptic malignant syndrome
Complication of treatment with antipsychotic drugs or withdrawl of dopamine agonists
Presentation of neuroepileptic malignant syndrome
Muscle rigidity
Autonomic instability
Hyperthermia
Altered mental state
Treatment of neuroepileptic malignant syndrome
Supportive measures
Ceasing of the responsible drug
Risk factors for neuroepileptic malignant syndrome
Dopamine disorders e.g. PD
Structural brain abnormalities
Genetics
Pathology of GBS
Segmental demyelination
Where do anti-Yo antibodies primarily occur?
In patients with paraneoplastic cerebellar degeneration (PCD) who have breast cancer or tumours of the ovary, endometrium and fallopian tube
Pathology of paraneoplasic cerebellar degeneration
Tumour cells express proteins normally expressed in the cerebellum, triggering an autoimmune reaction
S/Es phenytoin
Fatigue
Bone pain
Tingling and numbness in lower limbs
Gum hypertrophy
Antibodies of lambert eaten myasthenic syndrome (LEMS)
Anti voltage gated calcium channel Ab
Antibodies of myasthenia gravis
Acetylcholine receptor ab
When does labert eaten syndrome most often occur
As a paraneoplastic phenomenon - particular assosiation with small cell lung cancer
Reflexes - LEMS vs MG
LEMS - absence of reflexes
MG - reflexes unaffected
Autonomic features - LEMS vs MG
LEMS - autonomic features present
MG - uncommon
Fatgiue - LEMS vs MG
In contrast to MG, LEMS - temporary increase in muscle power post exercise
Treatment of LEMS
2,4-diaminopyradie (DAP)
IV immunoglobulins
and/or plasma exchange
Treatment of underlying cancer
Features of idiopathic intracranial HTN
High pressure headache
Worse on lying flat
Worse in the morning
Assosiated with papilloedema
What should be excluded if you are suspecting idiopathic intracranial HTN
Cerebral venous sinus thrombosis
Diagnosis of spontaenous intracranial hypotension
CSF opening pressure at LP (low)
CSF analysis NORMAL
MRI - diffuse pachymengineal enhancement, frequently in assosiation with sagging of the brain, tonsilar descent and posterior fossa crowding
Treatment of spontaenous intracranial hypotension
Conservative
Epidural blood patch
Is the headache better or worse lying down in spontaenous intracranial hypotension
Better lying down
Test for bradykinesia
Finger pinch test
Treatment of essential tremor
Propranolol
Primidone
What is tinels sign
Symptoms reproduced when tapping over the medial nerve
Seen in carpal tunnel syndrome
3 rules of the effects of paresis on diplopia
- Direction in which the distance between the images is at a maximum in the direction of the action of the paretic muscles
- Paresis of the horizontally acting muscles tends to produce mainly horizontal diplopia
- The image projected further from the centre belongs to the paretic eye
Which arteries are most commonly affected by thromboembolic disease in lateral medually syndrome
Vertebral or posterior inferior cerebellar arteries
What is multifocal motor neuropathy with conduction block closely related to
Chronic inflammatory demyelinating polyneuropathy
Antibodies of multifocal motor neuropathy with conduction block
Anti-GM1 antibodies
Presentation of multifocal motor neuropathy with conduction block
Asymmetrical motor neuropathies - usually in the upper limb
Reflexes may be preserved or slightly elevated at the onset of disease (causing frequent misidentification with MND)
Electro diagnostic hallmark of multifocal motor neuropathy
Motor conduction block
When would you do a sural nerve biopsy
If suspecting a vasculitc neuropathy
Presentation of progressive muscular atrophy (subtype of MND)
Lower motor neurone weakness distal upper and lower limbs
Without sensory loss
What does an upper motor neurone area involve
Brain
Spinal cord
What does a lower motor neurone area involve
Anterior horn cell
Motor nerve roots
Peripheral motor nerve
Signs of an UMN lesion
Disuse atrophy (minimal) or contractures
Increased tone (spasticity/rigidity) +/- ankle clonus
Pyramidal pattern of weakness (extensors weaker than flexors in arms, vise versa in legs)
Hyperreflexia
Upgoing plantars (Babinskis sign)
Signs of a LMN lesion
Marked atrophy
Fasiculations
Reduced tone
Variable pattern of weakness
Reduced or absent reflexes
Downgoing plantars or absent response
Presentation of primary lateral sclerosis (subtype of MND)
UMN weakness
Spascitity
Hyperreflexia
More likely to have bulbar involvement
Predominant symptoms of progressive bulbar palsy (subtype of MND)
Speech and swallowing difficulties
Presentation of sagital sinus thrombosis
Seizures
Focal neurological deficits
Predisposing factors for saggital sinus thrombosis
Dehydration
Haematological disorders
- anti-phospholipid, thrombophilia, protein S deficency, antithrombin III deficiency, thrombocythaemia, polycythaemia
Systemic conditions
- SLE, carcinoma, Behects disease, sarcoidosis, nephrotic syndrome
Local infections e.g. mastoiditis
What does botulism show on electromyography
Repeitive nerve stimulatio
What gene is mutated in huntingtons disease
Huntington gene (HTT)
Features of cavernous sinus syndrome
Eye muscle weakness
Proptosis
Chemosis (swelling of conjunctiva)
Horner syndrome
and/or facial sensory loss
Key structures that run through the cavernous sinus
CN III (oculomotor)
CN IV (trochlear)
CN V1 and V2 (opthalmic and maxillary divisions of the trigeminal nerve)
CN VI (abducent)
Sympathetic plexus surrounding the internal carotid artery
Cavernous part of the internal carotid artery
Presentation of vertebral artery dissection
Neck pain
Symptoms of posterior circulation stroke
What is the most common hereditary ataxia
Friedrichs ataxia
Pathology of friedrichs ataxia
Degeneration of the cerebellum, certain spinal cord tracts and peripheral nerves
Presentation of fredrichs ataxia
Ataxia
Dysarthria
Optic atrophy
Hearing impairment
LDs
Sensory neuropathy
Extensor plantar responses
Diabetes
Cardiomyopathy
Pes cavus
Kyphoscolosis
What is the most common type of partial seizure
Temporal lobe epilepsy
Presentation of temporal lobe seizures
Subjective abdo symptoms
Staring
Lip smacking
Period of disorientation
How is the vestibulo-ocular reflex tested
Caloric test
- monitoring of eye movements during or following the slow injection of at least 50ml of ice cold water over 60s into each external auditory meatus in turn
Where is the lesion if the vestibulo ocular reflex is negative
Brainstem
Treatment for generalised tonic clonic seizures
Sodium valpriate
Carbamazepine
Lamotrigine
Treatment for focal seizures
Carbamazepine
Lamotrigine
Treatment for abscence seizures
Ethosuximide
Treatment of GBS
Plasma exchange therapy
IV immunoglobulin
CSF analysis of GBS
Albuminocytolocigal dissociation (i.e. elevated protein)
However may be entirely normal
What features make up aphasia
Fluency
Repetition
Comprehension
Where is Brocas area and what is it for
Inferior frontal lobe
Centre for the motor part of speech and sentence formation
EXPRESSIVE DYSPHASIA
lesions - imparied fluency, intact comprehension and impaired repetition
Where is wernickes area and what is it for
Posterior, superior temporal lobe
Centre for comprehension and planning words
Lesions - cannot understand written or spoken words, speech remains fluent but meaningless RECEPTIVE DYSPHASIA
Treatment of filles de la tourette sydnrome (rare - mutliple tics with both motor actions and vocalisations)
Risperidone
Visual field testing results of indiopathic intracranail HTN
Loss of visual acuity when changing posture
Enlargment of blind spots and circumferential restriction in visual fields
Papilloedema
Most common cause and subsequant treatmnet of a 6th CN palsy
Microvascular nerve palsy (benign prognosis)
Vascular risk be addressed
Review in 4 weeks
What CNs pass through the pons
Facial nerve
Abducens
What does cervical radiculopathy refer to
One nerve root
What is synringomyelia
Sensory loss over a cape like distribution over the upper body, rather than peripheral sensory loss
What happens to cause syngobulbia
A synrinx forms in rhe brainstem
Typical CT findings of HSE
Hypodense areas in temporal lobes
Features of an extradural haemorrahage
Injury
Brief loss of consciousness
Recovery (lucid interval)
Delayed deterioration
What causes an extradural haemorrhage
Ruptures the middle meningeal artery (trauma)
Features of von hippel lindau (VHL) syndrome
Cerebellar haemangioma
Retinal angioma
Pancreatic and/or hepatic cysts
Adrenal and renal tumours
WHen do cluster headaches often occur
Nighttime
Assosiated symptoms with cluster headache
Runny nose
Watery eye
ptosis
WHat can bilateral bells paly sometimes be the first presenting symptom of
guillian barre syndrome
What condition is interferon B liscened for
RRMS who are able to walk unaided
Definition of RRMS
At least 2 attacks of neurological dysfunction (relapses) over the previous two years
How to test for CJD
LP
Presentation of new variant CJD in young adults
Psychiatric symptoms
followed by
- non specific painful sensory symptoms - most often in lower limbs
Cognitiv impairment
pyramidal signs
myoclonus
primitive relfexes
MRI findings of new variant CJD
High signal on T2 weighed imagines in the pulvinar (posterior aspect of the thalamus)
What are dorsal midbrain lesions assosiated with
Failure of vertical gaze
WHat controls vertical eye movements
Bilateral control of the cortex and upper brainsteam
Treatment of trigeminal neuralgia
Anti convulsants e.g. carbamazepine
What is hemibaslism
kinetic movement disorder
violent involuntary limb movements on one side of the body
WHat does hemibasilsm occur secondary to
Damage to the subthalamic nucleus (stroke, tumour, abscess)
Treatment of hemibasilsm
Dopamine antagonists
Treatment of cluster headache attacks
Sumatriptan injection
Oxygen inhalation
Prevention of cluster headaches
Verapamil
Lithium
Presentation of classic synringomyelia
Comonly assosiated with Arnold CHairai malformation and presents at 20-30 yrs of age
Upper limb pain excerbated by coughing or laughing
Pain and temp loss leads to painless upper limb burns and trophic changes
Difficulty in walking and paraparesis develop later
Gradually progressive condition
What is suggestive of an axonal neuropathy on a nerve conduction studies
Reduced compound muscle action potential amplitude
Myelin disorders nerve conduction studies
Reduction in velocities or blocks
Axonal disorders nerve conduction studies
Loss of action potential size/amplitude
WHat drugs commonly exacerbates weakness in myasthenia gravis
D-penicillaemine
Aminoglycoside and fluroquinolone antibiotics
Antiarrythmics e.g. quinidine, procainamide
B blockers e.g. propranolol
Neuromuscular blocking agents e.g. succinycholine
What is highly suggestive of spinal bulbar muscular atrophy (kennedy syndrome)
Perioral fasciculations
Androgen insensitivity