Neurology

Question 1

What domains make up the Glasgow coma score?

Answer 1

Eye Opening:

1. none
2. to pain
3. to speech
4. spontaneous

Best motor response:

1. None
2. extension to pain
3. flexion to pain
4. withdraws from pain
5. obeys commands

Best verbal response:

1. none
2. incomprehensible sounds
3. inappropriate words
4. confused
5. orientated

Question 2

What is the diagnosis of the worst headache of life in the back of head, coming on very quickly in a couple of seconds?

Answer 2

Subarachnoid haemorrhage

Question 3

What are the causes of sub arachnoid haemorrhage?

Answer 3

85% are from rupture of berry saccular (berry) aneurysms 
The rest are not due to aneurysms and may be due to:
arterial dissection 
AV malformation 
tumour
cocaine 
trauma 
septic aneurysm

Question 4

Where are the common sites for berry aneurysms?

Answer 4

Junction of posterior communicating artery with the internal carotid.
Junction of the anterior communication artery with the anterior cerebral artery.
Bifurcation of the middle cerebral artery

Question 5

What are the risk factors for berry aneurysms?

Answer 5

PKD, coaractation of aorta, Ehlers- Danons,

Question 6

What investigations help diagnose SAH?

Answer 6

CT detects >90% in first 48hrs
If CT is -ve but still clinically suspicisous can do an LP at 12hrs and will have xanthochromia (yellow colour from break down of blood)

+ve for red blood cells in the LP does NOT confirm SAH as it could be due to a bloody tap.

Question 7

How do you manage a SAH?

Answer 7

Referal to neuro surgery
Re examine neuro system often (GCS, pupils,)
Maintain cerebral pressure by keeping BP > 160mmHg
Nomodipine, a Ca channel antagonist, reduces vasopasm and decreases morbidity from the cerebral ischemia.

Surgery - coiling is better than clipping

Question 8

What are the complications of SAH?

Answer 8

Rebleeding - occurs in 20% in the first few days

Cerebral ischemia - due to vasospasm and may cause permanent deficit

Hydrocephalus - due to blockage of the arachnoid granulations

Hyponatraemia - is common, but do not manage with fluid restriction.

Question 9

Where is the blood coming from in a subdural haemorrhage?

Answer 9

Bleeding is usually from bridging veins between the cortex and the venous sinus.

The blood collects between the dura and the arachnoid layers.

Question 10

What are the risk factors for a subdural haeorrhage?

Answer 10

Men 
Age
Alcoholism 
Epilepsy
Anti coagulant therapy 
Thrombocytopenia 

Usually occurs after a minor fall

Question 11

Describe the changes seen on CT after a subdural:

Answer 11

The bleeding forms a sickle shape
The blood begins being hyperdense compared to the brain tissue, then in 2-3 weeks it becomes isodense an then after 3 weeks it becomes hypodense

Mid line shift may be present, and eventually the brain may herniate due to increased ICP

Question 12

What are the symptoms and signs of a subdural?

Answer 12

fluctuating level of consciousness, physical and intellectual slowing, sleepiness, headache, personality change, unsteadiness.

increases ICP, seizures, localising neuro symptoms occur late

Question 13

What classically cause extra dural bleeds?

Answer 13

Hit to the head over the parietal area damages the middle meningeal artery

Question 14

What are the changes on CT seen in an extra dural bleed?

Answer 14

Lens shaped haematoma, with a skull fracture and mid line shift

Question 15

What are the symptoms and signs of a extra dural bleed?

Answer 15

Initial LOC then recovers, followed by increasing drowsiness (lucid period)
Increasing headache, vomiting, confusion and fits. hemipariesis and ipsilateral pupil dilatation.

BP rises and HR decreases - Cushings response to increasing ICP.

Question 16

What is motor neurone disease?

Answer 16

A degenerative disease characterised by selective loss of neurones in the motor cortex, cranial n nuclei and anterior horn cells

Upper and lower motor neurones are affected but sensory cells are NEVER affected (helps to distinguish from MS and other polyneuropathies)
It NEVER affects eye movements (helps distinguish from myasthenia)

Fasiculations are very common!

Question 17

What are the 4 different clinical patterns of MND?

Answer 17

Amyotrophic lateral sclerosis (classic MND)
Loss of motor neurones and anterior horn cells in spinal cord - causes weakness with UMN signs and LMN wasting

Progressive bulbar palsy
Only affects cranial nerves IX - XII. LMN lesions of the tongue and muscles of talking and swallowing: flaccid fasiculating tongue, quiet hoarse voice.
Often progresses to ALS

Progressive muscular atrophy
Anterior horn cell lesions only - no UMN signs.
Affects distal muscle groups before proximal

Primary lateral sclerosis
Loss of Betz cells in the motor cortex - mainly UMN signs.
Marked spastic leg weakness and pseudo bulbar palsy (UMN lesions of muscles of swallowing and talking, slow tongue movements, slow deliberate speech, increased jaw jerk)

Question 18

How do you diagnosis ALS?

Answer 18

Clinical diagnosis - El Escorial diagnostic criteria

Definite = lower + upper motor neurone signs in 3 regions
Probable = lower + upper motor neurone signs in 2 regions
Probably with lab support = Lower + upper motor neurone sign in 1 region or UMN sign in >1 region + EMG shows acute denervation in >2 limbs
Possible = lower and upper motor neurone signs in 1 region
Suspected = upper or lower motor neurone sign in 1 or more regions

Question 19

What is myasthenia gravis?

Answer 19

Autoimmune disorder - antibodies to nicotinic acetlycholine receptors, results in fewer receptors on the post synaptic membrane so fewer neuromuscular transmissions can occur.

Question 20

What are the symptoms and signs of Myasthenia Gravis?

Answer 20

Increasing muscle fatigue - extraocular, bulbar, neck and shoulder girdle muscles are often affected first. Patients complain of double vision and ptsosis.
Tendon reflexes are normal

Anti AChr antibodies are raised in 90%
On repetative nerve stimulation a decremental muscle response is seen

If 50yrs more common in men and associated with thymic atrophy or thymic tumour.

Question 21

How do you treat Myasthenia Gravis?

Answer 21

1. Anticholinesterase (increases the amount of Ach around)
2. Prednisolone for relapses - can use azathioprine and methatrexate of needed
3. thymectomy

Question 22

What are the differentials for generalised muscle weakness?

Answer 22

MND - fasciculations
Muscular dystrophies - can be selective weakness and FHx
Dystrophia myotonica - ptosis, wasting of masseter, temporal and SCM muscles. May be gondal atrophy, and mental retardation. FHx. EMG diagnostic
Polymyositis - acute or chonic, skin rash and joint pains
Miscellaneous - thyrotoxic, hypothyroid, cushing’s, alcoholic
Non metastatic associations of malignancy - thymoma, small cell lung cancer (Eaton - Lambert)

Question 23

What are the causes of vertigo?

Answer 23

Peripheral (labyrinth and CVIII):
Benign positional vertigo -
due to debris in the semicircular canal
lasts for less than 1min at a time
occurs when moving head
Nystagmus on Hallpike manoeurve is diagnostic
the Eply manoeurve clears the debris

Vestibular neuronitis (acute labyrinthitis)
abrupt onset
N&V, no deafness or tinnitus
caused by viruses or vascular lesion
will settle on own

Meniere’s disease
endolymphatic hydrops causes recurrent attacks
each episode lasts >20mins
N&V, and tinnitus, and sensorineural hearing loss
Antihistamine can help

Ototoxicity
aminoglycosides, loop duiretics, cisplatin

Herpes zoster

Central - often have nystagmus 
Brainstem ischemia 
Posterior fossa tumours 
MS
Alcohol/ drugs 
Migraine
Epilepsy 
Acoustic neuroma - Schwannoma rises from the vestibular nerve. Unilateral hearing loss and vertigo. Ipsilateral V, VI, IX and X nerve involvement. VIII is not damaged until surgery

Question 24

What are the red flags when patients complain of a headache?

Answer 24

Worsening headache with fever - meningitis
Sudden onset reaching max intensity in 5mins - SAH
New onset neurological deficit
New onset cognitive deficit
New change in personality
Impaired LOC
Recent trauma
Worse when coughing sneezeing laughing - high ICP
Headache triggered by exercise
Headache that changes with posture
Symptoms suggestive of GCA or Acute angle glaucoma
Different to normal headache

Question 25

What are the recurrent/ chronic headaches and how do they differ from each other?

Answer 25

TENSION TYPE: Bilateral, pressing tightening, mild or moderate pain that doesn't aggravate with everyday activities No associated symptoms Lasts over 30 mins If 15 days per month = chronic tension type MIGRAINE: Usually unilateral but can be bilateral Pulsing, throbbing pain, moderate to severe that is aggravated or results in avoidance of everyday activities Associated with sensitivity to light and N&V Can have an aura Can last up to 72 hours If 15 days per month = chronic migraine CLUSTER: Unilateral, around face and eye. Stabbing, burning, throbbing pain that is severe and causes restlessness or agitation. Associated with red watery eye, nasal congestion, forehead sweating, ptosis on the same side as the headache. Can last between 15 - 180 mins 1 every other day with up to 8 in a day and more than 1 month of remission = episodic cluster 1 every other day with up to 8 in a day and not ever 1 month of remission for 12 months = continuous cluster. MENSTRUAL needs a headache diary to confirm headaches occur 2-3 days before menstruation for 2 or more consecutive cycles ANALGESIA OVERUSE: If a headache has become worse over 3 months of using paracetamol NSAIDs etc for more than 15days a month or triptans etc for more than 10 days a month.

Question 26

What are the differentials for an acute single episode headache?

Answer 26

With meningism: Meningitis Encephalitis SAH Head injury Subdural Extra dural Venous sinus thromobosis - causes increased ICP Sinusitis - pain worse when bending over Tropical illness - malaria Acute closed angle glaucoma

Question 27

What symptoms does trigeminal neuralgia give you?

Answer 27

Paroxysms of intense stabbing pain in the trigeminal area Usually uni lateral - triggered by washing hair, shaving, eating, talking Usually caused by an anomalous vessel close to the nerve causing compression of the trigeminal root

Question 28

What aspects of a history of blackouts would make you think someone was having an epileptic fit?

Answer 28

``` Attacks when asleep or lying down Aura Identifiable triggers (eg TV) Altered breathing Cyanosis Typical tonic clonic movements Incontinence of urine Tongue biting Prolonged post ictal phase Drowsiness, confusion, amnesia Focal paralysis (Todd's Palsy) ```

Question 29

What is epilepsy?

Answer 29

A recurrent tendency to spontaneous, intermitted abnormal electrical activity in part of the brain - manifested a seizures.

Question 30

What the causes of epilepsy?

Answer 30

2/3 are idiopathic Structural - cortical scarring from a head injury, developmental disorder (dysemryoplastic neuropathelial tumour), space occupying lesions, stroke, hippocampal sclerosis (after febrile convulsion), vascular malformation, Non epileptic causes of seizures: Trauma, stroke, haemorrhage, increased ICP, alcohol or benzo withdrawal, metabolic disturbance, liver disease, infection, fever, drugs and pseudosiezures

Question 31

How are seizures classified?

Answer 31

PARTIAL - focal onset with features referable to one part of a hemisphere Simple partial: awareness is unimpaired, focal symptoms with no post ictal phase Complex partial: awareness is impaired. May have simple partial (aura) onset, or impaired awareness from the onset. Usually from the temporal lobe. Partial seizure with secondary generalisation: after the initial partial seizure the electrical activity spreads more widely PRIMARY GENERALISED - simultaneous onset of electrical discharge throughout the cortex. No localising features. Absence: brief <10s, presents in childhood Tonic -Clonic: loss of consciousness, limbs stiffen (tonic) and then jerk (clonic), post ictal phase and drowsiness common. Myoclonic: sudden jerk of a limb face or trunk Atonic: sudden loss of muscle tone causing to fall, no LOC

Question 32

Multiple Sclerosis: What is is? How does it present? How is it diagnosed?

Answer 32

Relapsing and remitted demyelinating disease of the CNS. The plaques of demyelination occur at different sites, due to a T cell mediated response, unclear why. They heal incompletely causing the relapsing and remitting nature, with progressive neuronal loss. ``` The most common sites for plaques are: optic nerves periventricular region corpus callosum brainstem cerebellar connections cervical cord ```

Question 33

Multiple Sclerosis: What is is? How does it present? How is it diagnosed?

Answer 33

Relapsing and remitted demyelinating disease of the CNS. The plaques of demyelination occur at different sites, due to a T cell mediated response, unclear why. They heal incompletely causing the relapsing and remitting nature, with progressive neuronal loss. ``` The most common sites for plaques are: optic nerves periventricular region corpus callosum brainstem cerebellar connections cervical cord ``` It is diagnosed clinically, and requires lesions to be disseminated in time and space, and unattributed to other causes. The McDonald Criteria is used. MRI can show the lesions CSF shows olioclonal bands of IgG that are not present in the serum. Delayed Evoked potentials

Question 34

What are the symptoms of MS as it progresses?

Answer 34

``` Cognition decline, including memory Emotional liability Decreased mobility and increased fatigue Incontinence Pain Spasticity Oscilliopsia ```

Question 35

What is the definition of a TIA?

Answer 35

A sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation. Symptoms last

Question 36

What is amaurosis fugax?

Answer 36

Emboli in the retinal artery causing a curtain to descend over the vision in one eye.

Question 37

What are the causes of TIAs

Answer 37

ATHEROTHROMBOEMBOLISM: from carotids suspect if many episodes on the same side carotid bruit May need carotid endarterecomy if stenosis >70% CARDIOEMBOLISM: Mural thrombus post MI or in AF Need to anticoagulate HYPERVISCOSITY polycythaemia, sicklecell, high WCC, myeloma VASCULITIS cranial arteritis, PAN, SLE etc very rare ?actually a TIA

Question 38

What would lead you to an urgent referral to TIA clinic?

Answer 38

ABCD2 score >6 indicates stroke in 2 days high risk >2 need to be assessed within 24hrs Everyone else needs to be assessed within 72hrs ``` Age >60 = 1 point Blood pressure >140/90 = 1 point Clinical features: unilateral weakness = 2 points speech disturbances but no weakness = 1 point Duration : >1hr = 2 points 10-59 mins = 1 point Diabetes = 1 point ```

Question 39

What is Guillian Barre Syndrome?

Answer 39

Acute autoimmune inflammatory demyelinating polyneuropathy.

Question 40

What are the signs that would make you think a patient had Guillian Barre Syndrome?

Answer 40

Ascending weakness starting a few weeks after an infection, especially diarrhoea (campylobacter). Loss of reflexes, mild sensory symptoms, cranial nerve involvement, autonomic dysfunction Increased protein in CSF but not increased WCC. Slow conduction on nerve studies

Question 41

What test needs to be repeated regularly to monitor patients with Guillian Barre Syndrome?

Answer 41

FVC - needs to be checked every 4 hours to make sure that any respiratory muscle involvement is noted before it is difficult to intubate. If FVC 6 consider ventilating.

Question 42

Autonomic neuropathy: Causes Signs

Answer 42

Causes: Diabetes, GBS, HIV, paraneoplastic syndrome, leprosy, SLE, toxic, genetic Signs: Postural hypotension, erectile dysfunction or ejaculatory failure (Point and Shoot), less sweating, constipation, nocturnal diarrhoea, urine retention, Horner's syndrome, Holmes-Adies pupil

Question 43

What are the causes of polyneuropathy?

Answer 43

Mostly motor - Guillian Barre syndrome Lead poisioning Charcot Marie Tooth syndrome Mostly sensory - Diabetes renal failure Leprosy Others: Hypothyroidism, hypoglycaemia, mitochondrial disorders Vasculitides - polyarteritis nodosa, RA, wegeners Malignancy Infections - HIV, lymes Nutritional - low B12 (EtOH), low folate, high vit B6. Drugs - isoniazid, phenytoin, nitrofurantoin Amyloidosis

Question 44

What is the triad of parkinsonism?

Answer 44

Tremor - worse at rest Rigidity - superimposed with tremor to cause cogwheel Bradykinesia - slowness of movement initiation with progression to reduction in speed and amplitude of repetitive movements

Question 45

What are the causes of parkinsonism?

Answer 45

``` Idiopathic Multiple cerebral infarcts Parkinsons plus Post encephalopathy Drug induced - neuroleptics, prochlorperazine, metoclopramide Toxin induced Trauma ```

Question 46

What are the non motor features of Parkinson's disease?

Answer 46

``` Anosmia Depression Dementia Visual hallucinations Dribbling Postural instability REM behaviour sleep disturbance Mild urinary frequency and urgency L dopa side effects ```

Question 47

What medications can help in Parkinson's disease?

Answer 47

Levodopa (used with a dopa decarboxylase inhibitor) Dopamine agonists - delays using LDopa Anticholinergics - help tremor MAO-B inhibitors - used in early PD COMT inhibitors - may lessen OFF time

Question 48

Huntingtons disease: How is it inherited? How does the disease progress? What is the pathology?

Answer 48

It is autosomal dominant Early symptoms are insidious: slightly twitching of muscles, clumsiness, lack of concentration, short term memory loss, depression, changes in mood. It then progresses to chorea, dementia, fits and then death, within 15yrs of diagnosis. Cerebral atrophy, with loss of corpus striatum GABA and cholinergic neurones.

Question 49

What tracts do the different sensory modalities travel in the spinal cord?

Answer 49

Pain and temperature - spinothalamic | Joint position and vibration - dorsal columns

Question 50

What are the differences between upper and lower motor neurone lesions?

Answer 50

``` UMN lesions: Affects muscle groups Pyramidal - extension of the upper limbs and flexion of the lower limb Spasticity Hyperreflexia Up going plantars and clonus ``` LMN lesions: Wasting and fasciculation Hypotonia and reduced reflexes

Question 51

How is muscle weakness graded?

Answer 51

``` 0 - no muscle contraction 1 - flicker of contraction 2 - some active movement 3 - active movement against gravity 4 - active movement against resistance 5 - normal power ```

Question 52

Which areas of the brain do the different cerebral arteries supply?

Answer 52

Anterior - frontal ad medial part of cerebrum. Occlusion may cause weak, numb, contralateral leg and arm. Face is spared. Middle - lateral part of each hemisphere. Occlusion causes contralateral hemiparesis, hemisensory loss to face and arm. Contra lateral homonymous hemianopia Posterior - supplies occipital lobe Occlusion give contra lateral homonymous hemianopia with macula sparing.

Question 53

What are the different types of tremor and what causes them?

Answer 53

Resting tremor - abolished on voluntary movement. Seen in Parkinson's Intention tremor - irregular, large amplitude worse at the end of purposeful movement. Seen in cerebellar damage (MS, stroke) Postural tremor - absent at rest, present on maintained posture, my persist but is not worse on movement. Seen as benign essential tremor. Re - emergent tremor - postural tremor developing after a delay of ~10secs.

Question 54

What conditions cause chorea?

Answer 54

Huntingtons and syndenhams chorea (post strep infection)

Question 55

What are Hemiballismus?

Answer 55

Large amplitude, flinging hemi chorea contralateral to a lesion in the subthalamic nucleus

Question 56

What is a dystonia?

Answer 56

A prolonged muscle contraction causing abnormal posture.

Question 57

What are lacunar infarcts?

Answer 57

Small infarcts around the basal ganglia, internal capsule, thalamus and pons

Question 58

What are the causes of TIAs

Answer 58

ATHEROTHROMBOEMBOLISM: from carotids suspect if many episodes on the same side carotid bruit May need carotid endarterecomy if stenosis >70% CARDIOEMBOLISM: Mural thrombus post MI or in AF Need to anticoagulate HYPERVISCOSITY polycythaemia, sicklecell, high WCC, myeloma VASCULITIS cranial arteritis, PAN, SLE etc very rare ?actually a TIA

Question 59

What test needs to be repeated regularly to monitor patients with Guillian Barre Syndrome?

Answer 59

FVC - needs to be checked every 4 hours to make sure that any respiratory muscle involvement is noted before it is difficult to intubate. If FVC 6 consider ventilating.

Question 60

What are the non motor features of Parkinson's disease?

Answer 60

``` Anosmia Depression Dementia Visual hallucinations Dribbling Postural instability REM behaviour sleep disturbance Mild urinary frequency and urgency L dopa side effects ```

Question 61

When can thrombolysis be used in a stroke?

Question 62

What are the common causes of intracranial venous thrombosis?

Answer 62

``` Pregnancy Oral contraceptives Head injury Dehydration Blood dyscrasis Intracranial malignancy Extra cranial malignancy recent LP ```

Question 63

What is Ramsey Hunt syndrome?

Answer 63

VII nerve palsy associated with VZV in the auditory canal.

Question 64

What conditions causes momneuritis multiplex?

Answer 64

``` Wegner's, AIDS Amyloid Rheumatoid Diabetes Sarcoidosis PAN Leprosy Carcinomatosis ```