Flashcards in Neurology Deck (90):
What is benign positional vertigo? How is it diagnosed?
Due to canalolithiasis - debris in semicircular canal, disturbed by head movement, resettles causing vertigo lasting a few seconds after the movement
Nystagmus on performing hall pike maneouvre is diagnostic
How is acute labyrinthitis characterised?
Acute onset of severe vertigo, nausea, vomiting +/- prostration BUT NO deafness or tinnitus. Severe vertigo subsides in days, complete recovery takes 3-4 weeks.
What are the causes of acute labyrinthitis?
Infective - viral/bacterial
How is acute labyrinthitis managed?
Bed rest, anti-emetics.
What is Meniere's disease? (4)
Excessive fluid build up in the ear causing:
1. vertigo +/- N & V
2. sensorineural hearing loss
3. tinnitus with a sense of aural fullness
4. Drop attacks (Tumarkin's crises) - falling to one side without loss of consciousness
How is Meniere's managed? (3)
1. Bed rest and reassurance in acute phase
2. Prophylactic: low Na+ diet
3. Antihistamine if prolonged, or prochloperazine
List 3 drugs that can cause deafness +/- vertigo
How does an acoustic neuroma present? (3)
1. Unilateral hearing loss, with vertigo occurring later
2. With progression, nerves V, VI, IX and X may be affected (ipsilateral)
3. Signs of increasing ICP later
What is the difference in position between decorticate and decerebrate posturing?
Decorticate - flexes the arms up to the chest or 'core' of body
Decerebrate - extension of both arms and legs
Decerebrate = worse prognosis, indicates not only hemispheric dysfunction but also brainstem dysfunction
What is Wernicke's encephalopathy?
Caused by Vitamin B1 deficiency (part. in alcoholic patients). Characterised by confusion, gait ataxia and ophatlmoplegia.
What is the danger in giving glucose in Wernicke's encephalopathy and why?
Thiamin helps to breakdown glucose.
If glucose is given, this will rapidly consume the remaining thiamine reserves, exacerbating this condition
Therefore, glucose must be given CONCURRENTLY with thiamine, or AFTER thiamine is administered.
What is Korsakoff syndrome?
Persistent amnestic syndrome classically associated with confabulation and may follow Wernicke encephalopathy
What vitamin deficiency causes subacute combined degeneration?
Vitamin B12 (cyanocobalamin)
What are the clinical features of subacute combined degeneration? (4)
1. Hyporeflexia - sensorimotor neuropathy
2. Hyperreflexia - degeneration of the corticospinal tract in the CNS
3. Diminished proprioception and vibration sensation - degeneration of the dorsal columns of the spinal cord
4. Gait ataxia
What are four important causes of an organic headache syndrome/
(need to be ruled out - red flags!!)
When is a headache classified as a migraine? (3)
1. When the pain can be classified by at least two of the following: one-sided, moderate to severe, throbbing, aggravated by movement
2. At least one of the following associated symptoms: nausea, vomiting, photophobia, phonophobia
3. headache lasts between 4 - 72 hours
What is the difference between a classical or a common migraine?
Classical - migraine with aura (i.e. visual disturbances then vision normally restores itself)
Common - migraine without aura
What causes migraine?
1. Susceptibility is normally inherited
2. Current hypothesis - migraine caused by interaction between the brain and cranial blood vessels OR certain parts of brain hypersensitive to stimuli (e.g. emotion, bombardment with sensory impulses, any sudden change in internal or external environment)
Which medications can be used to abort the headache of a migraine attack? (2)
1. Triptans (serotonin agonists)
2. Ergotamin compunds - constrict cranial blood vessels
What five prophylactic drug therapies prevent or reduce the frequency of migraine?
2. Calcium channel blockers
3. TCAs - amitriptyline
4. Sodium valproate/valproic acid
What are the clinical features of a cluster headache? (4)
1. Excruciating, boring, burning pain (much more severe than migraine) localized around one eye - commonly radiating to forehead, temple, cheeck and upper gum on same side of face
2. Nasal congestion and lacrimation
3. Steady rather than throbbing pain
4. Attacks of 15-180 minutes, 1-3 attacks per day
When do clusters usually begin?
Which gender is most affected by cluster headache?
Distinguish the behaviour of a patient with cluster headache versus migraine headache
Patient with cluster headache paces; patient with migraine seeks solitude (dark room, sleep)
How are cluster headaches managed?
1. Avoid alcohol
2. Acute - ergotamine, intranasal lignocaine
3. Prophylactic - calcium channel blockers, corticosteroids
What are the clinical features of a tension headache? (4)
1. Dull, persistent pain that may vary in intensity and usually felt on both sides of head or neck - 'pressing/tight'
2. Tautness and tenderness of scalp, neck and shoulder muscles
3. Recurrent, episodic pain
4. Psychological: Trouble concentrating and difficulty sleeping
What is the presumed cause of pain in a tension headache?
Sustained cranial muscle contraction e.g. frowning or jaw-clenching
Can be triggered by poor posture, prolonged reading, emotions - stress/anxiety/fatigue
How is a tension-type headache managed? (2)
1. Pain relief - panadol, NSAIDs, or TCAs
2. Physiological - deep breathing exercises, neck and shoulder massage
What are the branches of the trigeminal nerve?
What are the clinical features of trigeminal neuralgia? (3)
1. Sharp, intermittent pain in the distribution of the trigeminal nerve - patient often winces - "tic doloureux"
2. Pain usually recurrent for weeks
3. Often triggered by chewing, drinking hot or cold fluids, shaving etc. Patients tend to avoid this.
Which medications are used to treat trigeminal neuralgia?
Anti-convulsants:carbamezapine, phenytoin, gabapentin
Where do the corticospinal tracts cross over and what clinical implications does this have?
Cross over at medulla - weakness is ipsilateral in corticospinal tract injury
Where do the dorsal column fibres decussate and what clinical implications does this have?
Decussate at medulla - loss of vibration/proprioception on same side as lesion
Where do the spinothalamic tracts decussate and what clinical implications does this have?
Fibres decussate 1-2 spinal nerve segments above point of entry (spinal cord) - loss of pinprick and temperature sensation on opposite side of lesion
What are the clinical features of hemi cord syndrome?
1. Loss of motor function below level on same side
2. Loss of vibration and proprioception on same side
3. Loss of temperature and pin prick on OPPOSITE SIDE
Do the lower limb myotome dance.
Hip F - L 2/3
Hip E - L 4/5
Knee E - L 3/4
Knee F - L 5/1
Dorsiflexion - L 4/5
Plantar flexion - S1/2
Inversion - L4
Eversion - L5/S1
Toes up - 5/1
Toes down 1/2
Compare the severity of muscle wasting in UMN vs LMN lesions
UMN - little
LMN - severe
Presence of fasciculations - UMN vs LMN lesions
UMN - none
LMN - maybe
In which type of lesion is clonus more likely to be present - UMN or LMN?
Sustained clonus in UMN
In general, how does one know which nerve root is affected by a disc protrusion?
Nerve root affected corresponds to vertebra immediately below the disc
Why can there be sacral sparing in central cord syndrome sometimes?
Sacral tracts are most lateral therefore can be unaffected in non-severe cases of central cord syndrome
Where is the neurological pathology in monocular blindness?
Lesion that occurs ipsilaterally between retina and chiasm
Where is the pathology in bilateral hemianopia?
Lesion at optic chiasm
What lesion(s) can give rise to a homonymous hemianopia?
Lesion behind optic chiasm OR lesion affecting both temporal and parietal optic radiations OR lesion affecting visual cortex
What lesion can give rise to a superior quadrantanopia?
Lesion of the temporal radiation (meyer's loop)
What is autonomic dysreflexia?
Syndrome of massive imbalance reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow - occurs after phase of spinal shock in which reflexes return
Peripheral hypertension occurs due to sympathetic discharge (usually bladder or bowel input) - brain attempts to shut down by sending inhibitory impulses + slows HR via vagus nerve BUT SCI prevents parasympathetic discharge from getting past that level
Therefore below level of SCI - sympathetics prevail. Above level - para sympathetics prevail (flushing/sweating etc.)
What are the clinical features of adult Klumpke's palsy? (4)
1. Claw hand
2. Paralysis of intrinsic hand muscles
3. Numbness in distribution of ulnar nerve
4. Involvement of T1 - Horner's syndrome
How can you differentiate between a L4/5 disc herniation and a common peroneal nerve palsy as a cause of foot drop?
L5 radiculopathy includes weakness of eversion and inversion alongside weakness of dorsiflexion (foot drop).
Inversion is generally spared in peroneal palsy because this function can be carried out by tib posterior (tibial nerve)
What are the afferent and efferent limbs of the corneal reflex?
Afferent - V1 (ophthalmic)
Efferent - VII - orbicularis - eye closure
Explain the pathophysiology behind the afferent pupillary defect.
When the torch shines on the normal eye, it and the contralateral eye constricts (normal response)
When the light is shone on the abnormal eye, both eyes paradoxically dilate
This is due to impairment of the afferent limb of the light reflex in the abnormal eye I.e. An optic nerve lesion
Describe the concept of pupil sparing in microvascular conditions
Fibres controlling pupillary function are superficial and spared from ischaemic injuries
What are the four different form of multiple sclerosis?
How is relapsing-remitting MS characterised?
Most common disease course of MS
Attacks of worsening neurologic function (relapses) followed by partial or complete recover periods (remissions)
How is secondary-progressive MS characterised?
Follows after relapsing-remitting course. i.e. disease will begin to progress more steadily with or without relapses
How is primary-progressive MS characterised?
Characterised by steadily worsening neurologic function from the beginning
How is progressive-relapsing MS characterisd?
Steadily progressive disease from the beginning and occasional exacerbations along the way
What is usually the first symptom of MS for many people?
Vision problems i.e. optic neuritis, etc.
What investigations are involved when MS is suspected? (3)
1. MRI - periventricular, juxtacortical, infratentorial or spinal cord
2. CSF - elevated lymphocytes and unmatched oligoclonal bands
3. Evoked potentials - demonstrate demyelination of optic pathways
How does one determine between an UMN vs LMN lesion in hemifacial weakness?
The lower motor neurons supplying forehead and part of obicularis oculi receive UMN from bilateral motor cortices
THERE IS OCCIPITALIS SPARING IN UMN LESIONS (because of bilateral cortical input - therefore if one UMN wiped out, the contralateral UMN can pick up the slack)
What's the difference between a partial and a generalised seizure?
Partial - occurs in just one part of the brain
Generalised - affect the whole brain
How are generalised seizures categorised?
Primary vs secondary
Primary - affects the whole brain from start of seizure
Secondary - starts as a partial seizure in one part of the brain and spreads to involve the whole brain
How are partial seizures categorised?
Simple - seizures do not affect consciousness
Complex - affect consciousness
Which artery supplies Broca's area?
Which artery supplies the Wenicke's area?
Which side parietal lesions produce more severe neglect?
Right parietal lesions = severe left neglect
Left parietal lesions = more subtle changes
How does Guillain Barre syndrome usually present?
Ascending weakness usually begins in the legs, moving upward to involve the arms. Weakness may be associated with or be preceded by mild distal paresthaesias
Usually rapidly progress over 1-4 weeks followed by a plateau phase that may last 2-4 weeks or longer
What are common antecedent illnesses to Guillain Barre syndrome?
Campylobacter jejuni gastroenteritis is the most common. Patients may have a preceding viral illness such as gastroenteritis or upper respiratory infection
What are the findings of neurologic examination of patients with Guillain Barre syndrome? (3)
Symmetric motor weakness that is usually greater in the distal extremities
Sensory function intact
How is Guillain Barre syndrome managed? (2)
1. Admission to hospital - close monitoring of respiratory function (complication: resp compromise, aspiration, arrhythmias and hypotension)
2. IVIG (better than plasmapharesis)
What is myasthenia gravis characterised by?
Autoantibodies against ACh R - weakness, vision problems, dysarthria (fatiguability, improvement after rest)
How is myasthenia gravis investigated? (3)
1. ACh R antibody levels in serum
2. Decremental muscle response to repetitive nerve stimulation
3. Ice test - ptosis improves after applying ice to shut eye for about 2 mins
How is myasthenia gravis managed? (3)
1. Anticholinesterase: pyridostigmine
2. Prednisolone +/- AZA
3. Possibly thymectomy (in younger patients)
Which three symptoms are used for diagnostic purposes in Parkinson's disease?
1. Tremor - most noticeable at rest and when stressed or tired
What is the pathology behind Parkinson's disease?
Degeneration of dopaminergic neurone, especially in the compact nigra
What pharmacological therapies can be used in the management of Parkinson's? (4)
1. levodopa +/- carbidopa or benzeraside (inhibits peripheral conversion of L-dopa to dopamine so there is more for brain)
2. COMT inhibitors - entacapone
3. MAO B inhibitors - selegiline
4. Dopaminergic agonists - bromocriptine, pramipexole
What is the pattern of symptoms seen in Huntington's?
Initially uncontrolled movement with motor impersistence, then loss of ability to initiate movement
What are the top 3 most common intracranial tumours?
What is a pure motor hemiparesis suggestive of?
List 3 differential diagnoses for a severe headache
List 3 differential diagnoses for ptosis
1. Oculomotor nerve dysfunction - secondary to PCOMM aneurysm, herniation, microvascular
2. Horner's syndrome
3. MG - fatiguability of muscle
What type of stroke causes contralateral hemiparesis that is more severe in the leg than in the upper limb?
What type of stroke cause contralateral hemiparesis that is worse in the face than in the leg?
Which symptoms characterise ALS/MND?
UMN and LMN signs but NO sensory loss or sphincter disturbance (distinguishes it from MS and polyneuropathies)
How would you work up a patient with suspected stroke?
1. Blood: FBE, UEC, lipids, ESR/CRP, fasting glucose
2. CT brain scan within 24 hours - distinguish between haemorrhage and infarct
3. ECG - look for AF
4. Carotid Doppler ultrasound if indicated - carotid stenosis
5. Echo - look for potential cardioembolic source
When is stroke thrombolysis indicated? (4)
1. Onset of symptoms within 0-4.5h (DO NOT THROMBOLYSE if patient wakes up from sleep with deficits)
2.CT scan confirmation of ischaemic stroke
3. Patient's neurological symptoms persist, not rapidly improving
4. Over 18
What is the ABCD2 score?
Predictor of risk occurring in the next 7 days after a TIA
A - Age more than 60 (+1)
B - Blood pressure systolic more than 140, diastolic more than 90 (+1)
C - Clinical feature: unilateral weakness (+2), speech disturbance without weakness (+1)
D - Duration (more than 60) (+2) (10-59) (+1)
D - Diabetes (+1)
High risk = 6-7
How would you manage a patient with TIA on discharge? (2)
1. Conservative: lifestyle, BP management, statins, stop smoking
2. Antiplatelet therapy (NOT TO be given if CT shows haemorrhage)
What is vertebrobasilar insufficiency?
TIA of the brainstem
What is the mainstay treatment for focal seizures?
("Car" - during a focal seizure you are more likely to still be able to drive a car compared to during a tonic-clonic)