Neurology Flashcards

Question 1

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Label the constituent portions of the cerebral cortex

Question 2

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Draw and label the circle of Willis and its branches

Question 3

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: List the cranial nerve nuclei in each constituent of the brainstem

Question 4

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the syndromes which would arise due to a lesion in - cerebral hemisphere, brainstem, cerebellum and basal ganglia

Answer

A

Cerebral hemisphere - Bulbar palsy, stroke/TIA

Brainstem - Pseudobulbar palsy

Cerebellum -

Basal ganglia - Parkinsonism and movement disorders

Question 5

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Name the location of the causative lesion in; Homonymous hemianopia; Homonymous quadrantanopia; Bitemporal hemianopia; Monocular visual field defect

Question 6

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the location of Broca’s and Wernicke’s area and explain their function in language

Answer

A

Location:

Broca’s - Frontal lobe of the left hemisphere
Wernicke’s area - Temporal lobe of the left hemisphere

Broca’s area - Motor function in speech. Infarct in this area leads to expressive dysphasia

Wernicke’s area - Involved in understanding language. Infarct in this area leads to receptive dysphagia e.g. able to formulate words as normal but not able to generate a sentence

Question 7

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: List the causes of dysarthria

Answer

A

Dysarthria: Occurs when there is a weakness in the muscles used for speech

Congenital
- Cerebral palsy
Acquired
- Stroke
- Head injuy
- Malignancy
- Progressive conditions e.g. Parkinson’s, MND

Question 8

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Explain the difference between bulbar and pseudobulbar palsy

Answer

A

Bulbar palsy: A LMN lesion of cranial nerves VII, IX, X and XII.

Causes: Polio, MND, syringobulbia, cerebrovascular events of the brainstem, GBS

Pseudobulbar palsy: A UMN lesion of cranial nerves IX, X and XII. Lesions affecting the corticobulbar tracts. Bilateral tract damage must occur for clinically evident disease, as the muscles are bilaterally innervated.

Causes: Cerebrovascular events, demyelinating events (e.g. MS), head injury

Bulbar palsy symptoms:

Absent/reduced gag reflex
Loss of swallow - may begin to drool
Fasciculations of the tongue
Flaccid paralysis
Absent/reduced jaw reflex
Nasal speech

Pseudobulbar palsy symptoms:

Brisk/normal gag reflex
Constant dribbling
Spastic paralysis of the tongue
Brisk/normal jaw reflex
‘Donald Duck’ voice
Bilateral UMN limb signs

Question 9

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: List the causes of Horner syndrome

Answer

A

Horner’s syndrome: Unilateral facial anhidrosis, partial ptosis, pseudoenopthalmos and miosis. Congenital Horner’s see iris heterochromia.

Causes:

Carotid artery aneurysm or dissection
Posterior inferior cerebellar artery or basilar artery occlusion
Pancoast tumour
MS
Cavernous sinus thrombosis
Hypothalamic lesions
Cervical adenopathy
Mediastinal masses
Pontine syringomyelia
Aortic aneurysm

Question 10

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the clinical features of UMN and LMN facial weakness

Answer

A

UMN: Forehead sparing - due to bilateral innervation to CN VII

LMN: Forehead also affected

Question 11

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Draw and label a cross section of spinal cord, with specific reference to spinothalamic pathways, corticospinal tracts and dorsal columns

Question 12

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the clinical syndromes that would arise from cord transection at C3, T10, cord hemi-section and posterior cord lesion

Answer

A

Cord transection at C3: Quadraplegia

Cord transection at T10: Paraplegia

Cord hemi-section: Brown-Sequard syndrome (ipsilateral loss of proprioception and vibration sensations, contralateral loss of pain and temperature sensation alongside ipsilateral limb weakness)

Posterior cord lesion: Loss of proprioception, vibration and light touch. (e.g. subacute combined degeneration (B12 deficiency), tabes dorsalis)

Question 13

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the clinical difference between upper and lower motor neuron limb weakness, with specific reference to findings on inspection, tone, deep tendon reflexes and pattern of weakness

Answer

A

UMN lesions:

Brisk reflexes
Increased tone
Spastic paralysis
Presence of primitive reflexes e.g. Babinski
Disuse atrophy

LMN lesions:

Absent/reduced reflexes
Reduced tone
Flaccid paralysis
Fasiculations
Severe atrophy

Question 14

Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Describe the clinical syndrome that would arise from S1 root lesion; C5 root lesion; Median nerve compression at the carpal tunnel; Ulnar nerve palsy; Peripheral neuropathy; Neuromuscular junction disorders; myopathy

Answer

A

S1 root lesion

Lumbar radiculopathy: Unilateral ‘shooting’ pain down the dorsal aspect of the leg in a dermatomal distribution (impingement of the nerve root), with radiation to the foot or toes.
There may be accompanying motor weakness in a corresponding myotomal distribution
Causes include intervertebral disc herniation, spondylolithiasis, spinal stenosis, infection or malignancy (metastasis)
Examination: Positive straight leg test

C5 root lesion

Cervical radiculopathy: Neck pain, with radiation down the arm, and numbness due to impingement of the cervical nerve root. Dermatomal distribution of pain
Causes include spondylosis, spondylithesis, disc herniation

Median nerve compression at the carpal tunnel

Carpal tunnel syndrome: Pain, tingling and weakness in the distribution of the distal median nerve. Pain may radiate up the forearm and wasting of the thenar eminence may be seen.

Phalen’s, reverse Phalen’s and Tinel’s test can be undertaken.

Ulnar nerve palsy

Damage at the elbow: Can occur due to compression of the ulna nerve at the medial epicondyle or in the cubital tunnel
- Motor function: All muscle innervated by the ulnar nerve are affected. Wrist flexion can occur, but only with abduction. Loss of digit abduction and adduction, thumb adduction is impaired (positive Froment’s sign)
- Sensory function loss
- Wasting of hypothenar eminence
Damage at the wrist: Such as due to laceration of the anterior wrist
- Motor function: Intrinsic muscle of the hand are affected
- Sensory loss: Only over the palm and fingers in the ulnar distribution. The dorsal branch is unaffected.

Peripheral neuropathy

Loss occurs in the distribution of the nerve, not in a dermatomal distribution
Diabetic neuropathy: Pain (typically burning) and loss of sensation in a ‘glove and stocking’ distribution
Shingles
Alcohol excess

Neuromuscular junction disorders

Myasthenia gravis
Botulism
Lambert-Eaton syndrome: Autoantibodies targeted against acetylcholine. Associated with small cell lung carcinoma.

Myopathy

Question 15

Q

LUMBAR PUNCTURE: Name the main anatomical landmarks used in guiding lumbar puncture and the coincident level in the spin

Answer

A

Pt on side with knees fully flexed to the chest.

Identify the iliac plane of the iliac crest (L3/L4)

Question 16

Q

LUMBAR PUNCTURE: Describe the two different positions a patient may adopt to undergo a lumbar puncture, and advantages of each with respect to ease of success and measuring opening pressure

Answer

A

Lying on side with knees flexed to chest
Sitting on the edge of the bed

Question 17

Q

LUMBAR PUNCTURE: List the potential complications of LP

Answer

A

Post-dural puncture headache (such as following a spinal block. Positional exacerbation - worse when upright)
Infection at site
Bleeding from site
Cerebral herniation *check for signs of raised ICP before proceeding*
Minor/transient neurological symptoms e.g. radiculopathy, paraesthesia
- Any lower body neurology after LP should be treated as cauda equina compression (haematoma, abscess) and an urgent MRI should be sought

Question 18

Q

LUMBAR PUNCTURE: List the contraindications to a lumbar puncture

Answer

A

Raised ICP (papilloedema, very severe headache, reduced consciousness, rising BP, vomiting, focal neurology) - CT prior to LP if suspected
Bleeding diathesis (prone to)
Cardiorespiratory compromise
Infection at site

Question 19

Q

LUMBAR PUNCTURE: List the acute clinical situations where a LP would be indicated

Answer

A

There are both diagnostic and therapeutic indications for LP:

Cerebrospinal fluid analysis (i.e. meningitis, multiple sclerosis, subarachnoid haemorrhage, GBS)
Spinal epidural (i.e. during labour)
Spinal medications (i.e. analgesia, chemotherapy, antibiotics)
Fluid removal (i.e. to reduce intracranial pressure)

Question 20

Q

LUMBAR PUNCTURE: Explain the term CSF xanthochromia

Answer

A

Xanthrochromia describes the yellow-ish appearance of CSF a number of hours (up to 12 hours) following bleeding. The yellow appearance is due to high protein levels within the CSF.

Question 21

Q

LUMBAR PUNCTURE: Explain the significance of CSF xanthochromia in a sudden onset headache

Answer

A

Highly suggestive of SAH, as bleeding occurs into the subarachnoid space.

The RBCs present in the CSF will also excite an inflammatory response, causing WCC to be raised (most marked after 48 hrs).

Question 22

Q

LUMBAR PUNCTURE: List the CSF findings that accompany multiple sclerosis

Answer

A

Raised protein content - oligoclonal bands, suggestive of intrathecal Ig production (which are not also present in the blood)

Paired CSF and serum samples are required for accurate interpretation.

If oligoclonal bands (IgG) are found in CSF and serum this suggests that the Igs have crossed into the CSF, as seen in conditions such as GBS, HIV infection and chronic inflammatory states (autoimmune diseases).

Question 23

Q

CT AND MRI: List the important contraindications to MRI

Answer

A

Metal implants or fragments

Question 24

Q

STATUS EPILEPTICUS AS A NEUROLOGICAL EMERGENCY: Define status epilepticus and describe initial investigations and components of management, including airway protection and use if anti-convulsants

Answer

A

Status epilepticus: A convulsive seizure lasting for 5 minutes in duration or recurrent seizures with no recovery in between (?3 seizures in 1 hour).

Initial investigations

A-E approach
- Secure patency of the airway and give high flow oxygen
- Assess cardiac and respiratory function (ECG, SpO₂)
- Check blood glucose levels
Obtain IV access, fluid resuscitate is necessary
- Urgent bloods and VBG

Management

Pharmacological treatment:
- 1st line: 4mg IV lorazepam. Repeat after 5 minutes if there is no response
- If no response within 20 minutes, IV levetiracetam, phenytoin or sodium valporate can be administered
- In the community: Buccal midazolam or rectal diazepam may be used

Question 25

Q

SPINAL AND ROOT EMERGENCIES: Describe the clinical presentation of; Acute compression of the cauda equina; Acute lesion of the thoracic cord; L5/S1 root impingement due to disc prolapsed

Answer

A

Acute compression of the cauda equina

Symptoms:

Bilateral shooting/burning down the dorsal aspect of the lower limbs, with radiation to the feet
Saddle anaesthesia
Loss of anal tone
Incontinence
- Urinary overflow incontinence
Sexual dysfunction: Inabilty to sustain an erection or ejaculate. Loss of sensation to the genitals

Signs:

Loss of anal tone on PR
Loss of sensation below the level of compression (dermatomal)
Reduced power below the level of the lesion (myotomal)
LMN signs below the site of the lesion e.g. reduced knee reflex if occuring at L2

Causes of cauda equina/cord compression: Disc herniation (central for cauda equina), malignancy (?mets), abscess/discitis, haematoma, spinal stenosis (spondylosis, spondolitheasis).

Acute lesion of the thoracic cord

Symptoms

Spastic paralysis - disturbance in gait
Loss of sensation

Signs

LMN signs at level of compression and UMN signs below level of compression: Hyper-reflexia, spastic paralysis, primitive reflexes present
Sensory loss below the level of the lesion

L5/S1 impingment due to disc prolapse (lateral disc prolapse)

Symptoms

Unilateral lumbar radiculopathy felt on the dorsal aspect of the lower limbs, with radiation to the feet

Signs

Positive straight leg raise (pain reproduced between 30 - 70 degrees of hip flexion is suggestive of lumbar disk prolapse between L4-S1. Lower until pain settles and the dorsiflex the foot)
Sensory loss in a dermatomal distribution

Question 26

Q

SPINAL AND ROOT EMERGENCIES: Describe the management of a suspected cauda equina (cord syndrome)

Answer

A

Hx

Establish symptoms: Pain distribution, urinary¹ and bowel symptoms, sexual dysfunction
- Can establish if complete or incomplete cauda equina, as in incomplete there is no urinary incontinence but only altered urinary sensation
Establish RFs for compression e.g. Hx of back pain suggestive of stenosis, Hx of malignancy or diagnosed mets, fever/infection suggestive of abscess or discitis, any Hx of trauma

Examination

Tone, power, reflexes
- LMN lesion symptoms (as the cauda equina is formed by LMNs)
Sensation: Lower limb anaesthesia
PR examination to check anal tone and saddle sensation
Post-void bladder scan (check for retention)

Management

Provide analgesia
Contact senior to arrange for assessment
- ?high dose dexamethasone to reduce localised swelling
Arrange urgent MRI
Catheterise if indicated
Prepare for surgery (cord decompression): FBC, clotting, G&S, LFTs, U&Es,

1: Loss of desire to urinate or reduced ability to void. Poor stream and need to strain.

Ddx:

Radiculopathy (no faecal/urinary/sexual dysfunction)
Cord compression (characterised by UMN signs)

Red flag symptoms in cauda equina:

Bilateral sciatica

Severe or progressive bilateral neurological deficit of the legs, such as major motor weakness with knee extension, ankle eversion, or foot dorsiflexion.

Difficulty initiating micturition or impaired sensation of urinary flow, if untreated this may lead to irreversible

Urinary retention with overflow urinary incontinence

Loss of sensation of rectal fullness, if untreated this may lead to irreversible

Faecal incontinence

Perianal, perineal or genital sensory loss (saddle anaesthesia or paraesthesia).

Laxity of the anal sphincter.

Consider an assessment of anal tone but note that this does not need to be performed in primary care.

Question 27

Q

NEUROMUSCULAR EMERGENCIES: Describe the clinical signs which point to neuromuscular ventilatory compromise

Answer

A

Inspection

Reduced chest expansion

Auscultation

Reduced breath sounds

Investigations

Type 2 respiratory failure findings on ABG

Question 28

Q

NEUROMUSCULAR EMERGENCIES: Name the bedside respiratory test of most use in monitoring neuromuscular ventilatory function

Answer

A

Spirometry: Allows for FVC (> 0.8) and FEV₁(> 0.7) to be assessed

Peak flow

Question 29

Q

NEUROMUSCULAR EMERGENCIES: Describe the findings on arterial blood gas which reflect type II respiratory failure

Answer

A

Hypercapnia and hypoxia

Question 30

Q

HEAD INJURIES: After the assessment of airway, breathing, circulation, describe the assessment of a patient with head injury

Answer

A

C-spine immobilisation if indicated

Airway

GCS of 8 or less leads to risk of inabilty to maintain own airway. Anaesthetist must be called immediately to assist with airway management
Suspected C-spine injury → jaw thrust
Caution in the use of airway adjuncts if there is extensive facial trauma

Breathing

Secure airway and provide oxygen

Circulation

Consider if fluid resuscitation is required
- Following head injury there is loss of cerebral blood flow autoregulation, now becoming reliant on SBP. For this reason it is vital to maintain SBP.

Disability and Neurological examination

Calculate GCS (E, V, M) - repeat every 30 - 60 minutes
Check pupillary responses and pupil size
Check blood glucose levels

Exposure

Look for evidence of facial fractures or depressed skull fractures
Check for evidence of basal skull fractures, such as racoon eyes, Battle’s sign, CSF discharge from the nose or ears or haemotympanum

Investigations

CT head +/- CT of the cervical spine

Question 31

Q

HEAD INJURIES: List the features which reflect severe head injury

Answer

A

Features of severe head injury

Impaired consciousness level (GCS < 13 or < 15 2 hours after the injury)
Fixed and dilated pupils
Basal skull fracture
Focal neurological deficit or visual disturbances
Seizures or amnesia
Significant headache or nausea and vomiting

Signs of neurological deterioration: Falling GCS, change in pupil size/responsiveness, development of focal neurological signs, changing respiratory rate, falling pulse, rising BP

Question 32

Q

EXTRADURAL HAEMORRHAGE AS A NEUROLOGICAL EMERGENCY: Describe the clinical presentation of an extradural haemorrhage

Answer

A

!!! EMERGENCY !!!

Affected vessel: Arterial vessels. Commonly the middle meningeal artery at the pterion

Hx:

Trauma to the head
Initial loss of consciousness followed by a _lucid period_ before further deterioration
Headache
Nausea and vomiting
Progressive drowsiness
Seizures in late stage

Examination

Focal neurology (aphasia, visual field defects, numbness, ataxia)
Signs of increased ICP
- Bradycardia +/- hypertension
- Fixed, dilated pupils
Symptoms of UMN lesion
- Hemiparesis
- Hyper-reflexia

Question 33

Q

EXTRADURAL HAEMORRHAGE AS A NEUROLOGICAL EMERGENCY: Describe the acute investigation and management of a suspected extradural haemorrhage

Answer

A

Acute investigation

Neurological examination
Routine urgent bloods: FBC, U&Es, CRP, clotting, G&S
CT head
- Hyperattenuated biconvex lesion seen (extra axial bleed)

Management

IV fluids to preserve cerebral perfusion
? Osmotic diuretics (e.g. mannitol) for relief of cerebral oedema
Surgical intervention - craniotomy
- >30cm³ require surgical management
Conservative management may be considered for ‘small’ extradural haematomas
- <30cm³ with low thickness, minimal midline shift and GCS > 8 without focal neurological deficits
- Involves serial CT imaging and neurological observation

Question 34

Q

BASE OF SKULL FRACTURE AS A NEUROLOGICAL EMERGENCY: Describe the clinical signs present in a fracture of the base of the skull

Answer

A

Racoon eyes
Battle’s sign
CSF leakage from the ears or nose
Haemotympanum (leading to conductive deafness)
Cranial nerve paralysis (VII and VIII - as they pass through the internal acoustic meatus)
- Other CNs may also be disrupted as they pass through their respective foramens, dependent upon the region of the skull base that is injured (anterior/middle/posterior fossa)

Question 35

Q

BASE OF SKULL FRACTURE AS A NEUROLOGICAL EMERGENCY: List the complications of a fracture of the base of the skull

Answer

A

Pneumocephalus from mask ventilation
Inadvertant placement of tubes within the cranium e.g. NG tubes
Carotid artery damage
Carotido-cavernous fistula

Question 36

Q

ACUTE HYDROCEPHALUS AS A NEUROLOGICAL EMERGENCY: Describe the clinical presentation of an acute hydrocephalus

Answer

A

Signs of raised ICP:
- Papilloedema, reduced consciousness, vomiting/nausea, severe headache, seizures, (paeds - ‘sun setting’, increase in head circumference and bulging fontanelle), bilateral pyramidal signs (spasticity, weakness, hyperreflexia, upgoing plantars)
- Symptoms typically worse in the morning, after a prolonged period of lying supine
NPH¹: ‘Wet, wobbly and wacky’ - incontinence, gait disturbance and confusion

1: NPH occurs following gradual blockage of the CSF drainage pathways in the brain. The venticles enlarge to handle the increased volume of CSF, which compresses the brain and eventually destroys tissue. Due to venticular enlargement there is little or no pressure increase in the majority of patients

Hydrocephalus may be described as communicating (reduced resorption by arachnoid villi) or non-communicating (blockage of CSF drainage from the ventricles to the subarchnoid space)

Question 37

Q

ACUTE HYDROCEPHALUS AS A NEUROLOGICAL EMERGENCY: List 3 patient groups at risk of developing acute hydrocephalus

Answer

A

Following brain insult:
- SAH
- Head injury
- Meningitis
Patients with congenital malformations (e.g. stenosis of the aqueduct of sylvius)
Posterior fossa/brainstem tumours

Brain insult (meningitis, SAH), congenital malformations → communicating hydrocephalus

Obstructing tumour/cyst, congenital malformations → non-communicating/obstructive hydrocephalus

Question 38

Q

ACUTE HYDROCEPHALUS AS A NEUROLOGICAL EMERGENCY: Describe the immediate investigation and management of suspected acute hydrocephalus

Answer

A

Immediate investigation

CT head:
- Findings include ventricular enlargement.
- With generalised enlargement suggestive of communicating e.g. secondary to meningitis or SAH
- Local dilatation suggestive of obstuctive.
- PC: Headache, N&V, symptoms worse on waking, altered GCS, reduced VA *features of raised ICP*

Management

Insertion of an external ventricular drain
Pharmacological CSF secretion inhibition: Furosemide and acetazolamide

Question 39

Q

MANAGEMENT OF THE SEMI-CONSCIOUS/UNCONSCIOUS PATIENT: Provide a differential diagnosis of a semi/unconscious patient

Answer

A

Vascular:

Stroke, SAH, shock, haematoma

Infective/inflammatory:

Sepsis, meningitis, encephalitis, abscess

Trauma:

Traumatic brain injury

Autoimmune:

Brainstem dmyelination

Metabolic:

Hyper/hypo: Glycaemia, calcaemia, natraemia
Hypo: adrenalism, thyroidism
Severe uraemia
Wernicke-Korsakoff syndrome
Hyper/hypothermia

Neoplasm:

Cerebral tumour

Others

Seizure
Substance abuse
Overdose

Question 40

Q

MANAGEMENT OF THE SEMI-CONSCIOUS/UNCONSCIOUS PATIENT: Describe the scoring system of the GCS, including the individual grades of each of the three domains

Answer

A

Eyes

4 Spontaneously open

3 Open in response to voice

2 Open in response to pain

1 No opening

Verbal

5 Orientated

4 Confused

3 Words

2 Noises

1 No verbal response

Motor

6 Obeys commands

5 Withdraws from pain

4 Localises to pain

3 Inappropriate flexion to pain

2 Inappropriate extension to pain

1 No response

Question 41

Q

MANAGEMENT OF THE SEMI-CONSCIOUS/UNCONSCIOUS PATIENT: Describe the clinical examination on a semi-conscious/unconscious patient, with specific reference to the initial assessment of ABC, and subsequent neurological and cardiological examinations

Answer

A

Clinical examination

A-E assessment

Ensure any major haemorrhage is controlled. Assess for risk of C-spine injury

Airway: Check patency. Perform jaw thrust if required. Airway adjuvants as indicated.

Breathing: RR, PaO₂, auscultate, percuss, check expansion, ABG

Circulation: Pulse, ECG, heart sounds, CRT

Disability: Glucose, pupils, GCS

Exposure: Check whole body

Neurological examination: General neuro and cranial nerves

Pupillary responses

Unilateral dilated pupil → ?raised ICP
Bilateral fixed, dilated pupils → brainstem death or deep coma
Pinpoint pupils → opiate overdose, pontine lesion interrupting the sympathetic pathway

Question 42

Q

MANAGEMENT OF THE SEMI-CONSCIOUS/UNCONSCIOUS PATIENT: Describe the investigation of the semi/unconscious patient

Answer

A

Bedside: ECG,

Bloods: FBC, U&Es, LFTs, CRP, blood cultures

Toxin screen (drugs and alcohol)

Imaging: CT/MRI head

Question 43

Q

MANAGEMENT OF THE SEMI-CONSCIOUS/UNCONSCIOUS PATIENT: Describe the immediate management of an unconscious patient, including the protection of the patient’s airway and maintenance of the patient’s circulatory pressure.

Answer

A

Signs indicative of airway obstruction in unconscious patients: Snoring/added noises, abnormal chest wall movements and lack of fogging on the oxygen mask

Suction
Chin-lift manoeuvre
Jaw thrust
Airway adjuncts
- Oropharyngeal airway (measure from the incisors to the angle of the jaw)
- Nasopharyngeal airway ! Avoid in basal skull fractures

Maintenance of circulatory pressure

Inotropes may be used to maintain BP, such as adrenaline, dobutamine, isoprenaline and ephedrine

Question 44

Q

CEREBROVASCULAR DISEASE: Explain the following terms, with specific reference to time course; Stroke; Transient Ischaemic Attack; Amaurosis Fugax

Answer

A

Stroke: Sudden onset focal neurological deficit, lasting for > 24 hours

TIA: Sudden onset focal neurological deficit lasting < 24 hours. Without signs of cerebral infarcation on MRI scanning.

Amaurosis fugax: Sudden onset, unilateral vision loss. Can be associated with ICA stenosis, ocular disease or migraine.

Question 45

Q

CEREBROVASCULAR DISEASE: List the irreversible and reversible factors leading toward the development of ischaemic stroke

Answer

A

Irreversible factors

Age
Gender
Hypercoagulable staes
AF

Reversible factors

Atherosclerosis: Diet, alcohol, DM
Smoking
Exercise levels
Lipid levels
Use of oestrogen containing oral contraceptives

Less common RFs: Endocarditis, migraine, polycythaemia, APL syndrome, vasculitis, amyloidosis

Question 46

Q

CEREBROVASCULAR DISEASE: Describe the risk factors, clinical presenting features and pathological causes and consequences of ischaemic and haemorrhagic stroke.

Answer

A

Posterior circulation strokes may be difficult to diagnose and should be suspected iF the person presents with:

Symptoms of acute vestibular syndrome —
- Acute, persistent, continuous vertigo or dizziness with nystagmus
- Nausea or vomiting
- Head motion intolerance
- New gait unsteadiness.

Question 47

Q

CEREBROVASCULAR DISEASE: List the clinical differences between a stroke which arises from anterior circulation territory and one which arises from posterior circulation territory

Answer

A

Anterior circulation stroke

Regions affected: Motor cortex, sensory cortex, temporal lobe (Wernicke and Broca’s area), striatum, internal capsule¹

Clinical signs and symptoms:

Contralateral paralysis
Contralateral loss of sensation
Aphasia if in dominant hemisphere (usually less)
Contralateral hemiparesis/hemiplegia

Posterior circulation stroke

Regions affected: Lateral corticospinal tract, medulla, pons, cerebellum, occipital cortex, visual cortex

Clinical signs and symptoms:

ASA: Lateral corticospinal tract infarct → contralateral hemiparesis (Medial medullary syndrome)
PICA: Lateral medulla → vomiting, vertigo, nystagmus, reduced pain and temp sensation (Lateral medullary syndrome - don’t pick a (PICA) horse (hoarseness) that can eat (dysphagia))
AICA: Lateral pons → affects on CN VII, VIII, V (Lateral pontine syndrome - facial droop means AICA’s pooped)
PCA: Occipital cortex, visual cortex → contralateral hemianopia with macular sparing
Basilar artery: Pons, medulla, lower midbrain etc → locked in syndrome (preserved consciousness and blinking)

1: Common location of lacunar infarcts, secondary to unmanaged hypertension

Question 48

Q

CEREBROVASCULAR DISEASE: Explain the Bamford classification of stroke, describing the prognostic difference between each stroke type

Answer

A

TACS: Proximal MCA occlusion

PACS: Distal MCA or ACA occlusion

POCS: PCA occlusion

THINK of cerebral territories supplied by each vessel, and therefore their corresponding deficits

Question 49

Q

CEREBROVASCULAR DISEASE: Describe the acute management of stroke, with particular attention to Examination; Investigations; Consideration or initiation of Antiplatelet therapy, Anticoagulation, Thrombolysis, Blood pressure control, Statin therapy

Answer

A

Acute management of stroke

Clinical Hx and examination
- !!! Establish timing of symptom onset
- Establish if there is any identifiable cause of the event e.g. AF (ECG), local atherosclerosis e.g. internal carotid (Carotid doppler), endocarditis (mumur), OCP, malignancy
- Look for RFs for haemorrhage e.g. anticoagulant use,
Once stroke is suspected administer 300mg aspirin
CT head required to rule out haemorrhagic stroke
Adminster thrombolysis if CT confirms ischaemic stroke AND symptom onset is within 4.5 hours
Ongoing monitoring of patient vitals, with importance placed upon management of blood pressure, glycaemic control and temperature
Upon discharge discussions surrounding pharmacological therapy should be had with the patient:
- Antiplatelet therapy - clopidogrel
- Statin
- Antihypertensive if required
- Anticoagulant if required. Should only be started after 2/52 following the event

Question 50

Q

CEREBROVASCULAR DISEASE: List the immediate non-pharmacological measures in management of stroke such as assessment

Answer

A

Assessment of swallow: Check swallow upon admission (cranial nerve assessment), SALT assessment should be performed
Rehabilitation
Nursing care

Question 51

Q

CEREBROVASCULAR DISEASE: Outline measures undertaken in secondary prevention of stroke

Answer

A

Antiplatelet therapy: Clopidogrel 75mg OD
Antihypertensive
Statin
Anticoagulant if required (AF)

Question 52

Q

CEREBROVASCULAR DISEASE: Outline methods of evaluating and managing patients with carotid stenosis

Answer

A

Evaluating carotid stenosis

Auscultate for bruits
Carotid duplex scan

Managing carotid stenosis

Endarterectomy
Angioplasty and stenting

Question 53

Q

CEREBROVASCULAR DISEASE: Outline medical and surgical management of TIA

Answer

A

Medical management

Acute: 300mg aspirin
Stroke prevention: Clopidogrel, statin, control BP, lifestyle modifications
Identify cause
- Carotid stenosis: Carotid doppler
- AF → anticoagulant

Surgical management

Treat carotid stenosis: Endartectomy or angioplasty and stenting
*

Question 54

Q

VENOUS SINUS THROMBOSIS: List the risk factors for the development of venous sinus thrombosis

Answer

A

Infection e.g. sinusitis, subdural empyema
Pro-thrombotic risk factors: COCP, pregnancy, malignancy, genetic thrombophilia
Head injury
Recent LP

Pathophysiology: Thrombus within venous sinuses → increased pressure within vessels and RBC breakdown → local ‘leakage’ of RBC into the surrounding cerebral tissue, causing a cerebral haemorrhage

Question 55

Q

VENOUS SINUS THROMBOSIS: Outline the clinical presentation of venous sinus thrombosis and how it differs from the presentation of arterial stroke

Answer

A

Clinical presentation *symptoms can depend upon the location of the thrombus*

Headache: May be sudden onset, as seen in SAH
Seizures
Impaired consciousness
Possible neurological signs
- Cranial nerve palsies
Papilloedema

Differentiating venous sinus thrombosis from cerebrovascular disease:

Seizures are seen in sinus thrombosis
Pts may have bilateral signs
There may be a progressive depression in consciousness
Signs and symptoms develop slowly, rather than sudden onset as in stroke.

Question 56

Q

SUBARACHNOID HAEMORRHAGE: Describe the clinical presentation of a subarachnoid haemorrhage, with specific reference to features in the history and examination including the rate of onset of symptoms, and signs arising from the event

Answer

A

Clinical presentation of SAH

Sudden onset, ‘worst ever’ headache
Onset related to times of physical exertion
Increasing drowsiness
Nausea/vomiting
Meningism - stiffneck, photophobia
Neurological deficit - 3rd nerve palsy, ophthalmic bleeds

Features in the Hx

RFs present: Hx of poorly controlled hypertension, berry aneurysms, arteriovenous malformations, PCKD
Meningism: Photophobia, neck stiffness, vomiting and nausea

Examination findings

Positive Kernig’s sign
Papilloedema

Ddx: Cerebral venous sinus thrombosis, SOL, head injury

Question 57

Q

SUBARACHNOID HAEMORRHAGE: Describe the vascular abnormalities which may predispose a patient to developing a SAH

Answer

A

Berry aneurysms: An acquired abnormality. Develop in the circle of willis and surrounding vessels.
- RFs for berry aneurysms include PCKD, HTN, FH, smoking and Erlers-Danlos/Marfan’s syndrome
Arteriovenous malformations: A congenital maformation of veins and arteries

Question 58

Q

SUBARACHNOID HAEMORRHAGE: Explain how one may investigate a SAH within the acute setting

Answer

A

Investigations

Examination: Neurological (peripheral and CN), Kernig’s and Brudzinski’s signs, perform fundoscopy

Bloods: FBC, U&Es, LFTs, CRP, clotting

Imaging: CT head (hyperattenuated regions seen)

LP: IF CT is normal. Should be performed > 12h after symptoms onset

CT/MRI angiography for all pts fit for surgery (allows for identification of the vascular abnormality)

Question 59

Q

SUBARACHNOID HAEMORRHAGE: Describe the acute management of SAH

Answer

A

Early management aims

Prevention of rebleeding
Prevention of delayed cerebral ischaemia due to vasospasm

Management

Endovascular obliteration via platinum spirals (coiling) OR clipping to prevent rebleeding. Systolic BP should be kept < 180mmHg before.
PO nimodipine and maintaining circulatory volume to reduce the risk of vasospasm.
- Hypertension should be controlled but should be high enough to maintain cerebral perfusion
Supportive management:
- Specialist referral - neurosurgery
- Assessment of swallow
Ventricular drainage if indicated (SAH complicated by hydrocephalus)

Question 60

Q

SUBARACHNOID HAEMORRHAGE: List the potential complications of a subarachnoid haemorrhage

Answer

A

Rebleeding
Death ~30% die immediately
Vasospasm (leading to insufficient cerebral perfusion and can cause clot formation within vessels, ultimately causing obstruction)
Hydrocephalus

Question 61

Q

SUBDURAL HAEMORRHAGE: List the predisposing factors which make a patient vulnerable to developing subdural haemorrhage

Answer

A

Trauma (acceleration-deceleration injury)
Elderly
ETOH excess
Anticoagulant use
Clotting abnormalities (haemophilia)

Question 62

Q

SUBDURAL HAEMORRHAGE: Describe the clinical presentation of a chronic subdural haemorrhage

Answer

A

Chronic subdural haemorrhage = 15+ days following traumatic precipitant. Most common in the elderly population.

Signs of raised ICP: Confusion, progressive headache, nausea/vomiting, focal neurology (limb weakness, dysphasia) PLUS cranial nerve palsies, assymetrical pupils
May accompanied by anorexia
Hx of trauma +15 days previous - may be ‘trivial’ so be sure to employ specific questions

Examination findings

?Pupil dilation and fixation if raised ICP
Cranial nerve palsies (raised ICP)
Papilloedema
Limb weakness
Abnormalities of speech
May progress to Cushing’s triad if ICP exceeds MAP (bradycardia, increased pulse pressure/BP and Cheyne-Stoke’s breathing)
Tense fontanelle in babies

Question 63

Q

SUBDURAL HAEMORRHAGE: Describe the CT scan appearance of a subdural haemorrhage and how it would change withtime

Answer

A

CT scan appearance

Crescent shaped lesion
Crosses suture lines
May be midline shift (dependent upon ICP - may see ventricular compression)

Changes over time

Hyperdense → hypodense
?Increase in size
May change shape from cresenteric to convex (similar to extra dural haematoma appearance)

Question 64

Q

SUBDURAL HAEMORRHAGE: Describe the management of a patient once a subdural haemorrhage is detected, with specific reference to who’s advice should be sought

Answer

A

Subdural haemorrhage management (acute and chronic)

Seek neurosurgery review
- Emergency craniotomy and clot evacuation
Alert senior
Treatment of raised ICP¹ using mannitol infusion
- Elevate head
- Maximise oxygenation
- BP management - allow ‘permissive hypertension’ with systolic of at least 140mmHg (allows for adequate cerebral perfusion pressure)
Small and asymptomatic haemorrhages may be managaed with observation and serial CT

1: Asymmetrical pupils, cranial nerve palsies, Cushing’s triad

Answer 60

A

Micro-aneurysms
Anticoagulants
Hypertension

Answer 61

A

Clinical presentation

A.K.A. haemorrhagic stroke
Signs on raised ICP: Unequal pupils, cranial nerve palsies, headache, nausea/vomiting
As per ischaemic stroke
- LAC: Pure sensory stroke, pure motor stroke, hemisensory stroke, ataxic hemiparesis

Initial investigation

CT head (hyperdense regions with surrounding hypodensity (associated oedema) seen)
Peripheral and cranial nerve examination
Fundoscopy (?papilloedema)
ABG

Immediate patient management

Manage raised ICP: IV mannitol, head elevated, maximum oxygenation
Control BP (<140/90 within 1 hour) - amlodipine, labetalol, betolol
Reverse anticoagulant if applicable
Neurosurgical referral

Answer 62

A

Red flag features of headache

Pain worsened by laying down/worse on waking (?raised ICP)
Associated nausea/vomiting (?raised ICP)
Severe, sudden onset (?SAH)
Associated meningism (photophobia, neck stiffness)
Progressive and persistent
Focal neurological signs e.g. cranial nerve palsies (?raised ICP)
Associated systemic illness suggestive of infection

Appropriate investigations

SAH: CT head, fundoscopy
- Raised ICP: Cranial nerve examination, pupil responses, fundoscopy, vitals (check for Cushing’s triad)
Meningitis: LP, blood cultures
Temporal arteritis: Biopsy

Should include headache of Subarachnoid haemorrhage (see stroke/ cerebrovascular disease), Meningitis/Encephalitis (see CNS infection), and Raised Intracranial Pressure

Answer 63

A

Epidemiology:

F>M
Patients > 50 years old

Associated conditions:

Polymyalgia rheumatica
Hip and shoulder girdle aching
Morning stiffness

Answer 64

A

A systemic large and medium vessel vasculitis.

Cause unknown but thought to be autoimmune mediated.

Can involve other branches, such as the ophthalmic artery. This can lead to arteritic AION or PION (anterior or posterior ischaemic optic neuropathy) or central retinal artery occulusion. This in turn leads to vision loss.

Answer 65

A

Associated clinical features:

Headache
Jaw claudication
Pain worsened by jaw movement e.g. eating
Scalp tenderness e.g. when brushing hair
Amaurosis fugax or sudden onset unilateral vision loss
Bilateral visual loss *late stages*

Associated symptoms and signs:

Palpable, inflammed temporal artery on examination
RAPD (due to optic nerve ischaemia)
General malaise, weight loss, morning stiffness
Unequal pulses in each arm (due to involvement of the aortic arch, leading to aneurysm, dissection or stenosis)

Answer 66

A

Examination: Palpable temporal artery, check vision (AFRO), check radial pulses, cranial nerve examination

Investigations

Temporal artery biopsy within 2/52 of starting steroids
- Skin lesions can occur and hence a negative biopsy doesn’t rule out the dx
CRP/ESR ↑↑
Platelets ↑
ALP ↑
Hb ↓

Answer 67

A

STEROIDS

PO Prednisolone 60 mg

OR - if there is ophthalmic involvement:

IV methylprednisolone (evolving visual loss of Hx of amaurosis fugax)

Typically requires a 2 year course.

Consider complication of steroids and required prophylaxis e.g. PPI, bisphosphonate and calcium with colecalciferol (Vitamin D).

Answer 68

A

Bilateral visual loss

Answer 69

A

Space occupying lesion
Intracranial haemorrhage (including stroke - intracerebral)
Hydrocephalus
Abscesses or infection: Meningitis
Idiopathic intracranial hypertension

Answer 70

A

Pain worse on:
- mornings/after laying down
- coughing or after bending forwards
Progressive worsening of pain
Associated vomiting
Not relieved by analgesia
Associated visual symptoms: Loss of peripheral fields of vision

Answer 71

A

Ophthalmic findings:

Pupil asymmetry/abnormalities
- Constriction in early stages, then dilated
Papilloedea *not that reliable*
- Absent venous pulsation at the optic disc
Vision loss - peripheries of visual field

Vital signs

Cushing’s triad (hypertension/increased pulse pressure, bradycardia and cheyne-stokes breathing)

Neurological

Altered GCS
Focal neurology

Answer 72

A

Coning (Cushing’s triad is indicative of this)
Vision loss
Altered consciousness
Personality changes
- !!!! Be especially aware of this in elderly pts as a false diagnosis of dementia may be made, be sure to ask about hx of trauma in past few months as they may be suffering from a chronic subdural haematoma

Acute Mx

Reduce ICP using IV mannitol
Reduce PaCO₂ through hyperventilation (causes vasoconstriction - immediately reducing ICP)
BP management: Keep systolic > 180 mmHg to maintain cerebral perfusion
Elevate head
Temperature control
Cranitomy for resolution

Answer 73

A

*Dependent upon the location of the lesion

Signs of raised ICP: Headache (think of characteristic features), vomiting, cranial nerve palsies (e.g. CN III and VI, ptosis), papilloedema/absent venous pulsation on fundoscopy
Altered mental state
Seizures

Answer 74

A

Paraneoplastic syndrome: Triggered by an abnormal immune response to a neoplasm. Consists of symptoms which are attributable to a malignancy mediated by hormones, cytokines or the cross reaction of tumour antibodies. They do not correlate with stage/prognosis.

Myasthenia gravis - seen in thyoma and bronchogenic carcinoma
Subacute cerebellar syndrome - ovarian cancer
Paraneoplastic limbic encephalitis³
Neuropathy² - seen in lung, breast, myeloma, Hodgkin’s and GI
Lambert-Eaton myasthenic syndrome¹ - mostly lung (SCLC)

1: Muscle weakness etc due to autoantibodies against the pre-synaptic calcium channel receptor. Weakness improves with activity.

2: May be peripheral, autonomic or cerebellar
3: Sees changes in personality/mood, problems sleeping and changes in short term memory

Answer 75

A

Glioma

Astrocytoma
- Glioblastoma multiforme is the most common. Grows rapidly, presenting with signs of raised ICP (headache, cranial nerve palsies (III, VI), nausea, Cushing’s triad)
Oligodendroglioma
Ependymoma
- Most common in children/young people
- Usually malignant

Meningioma

Usually benign but their size can cause mass effect, leading to increased ICP
Most common overall cerebral neoplasm

Pituitary tumours

Can cause compression of the optic chiasm, leading to bitemporal hemianopia

Acoustic neuroma

Present with unilateral sensorineural deafness, tinnitus, vertigo and facial palsy
Affect CNc V, VII and VIII
Growth of the tumour can cause cerebellar symptoms or bulbar palsy
Bilateral acoustic neuromas are associated with neurofibromatosis type 2

Answer 76

A

Bronchus
Breast
Kidney
Colon
Thyroid
Malignant melanoma

Answer 77

A

‘Wet, wobbly and wacky’

Urinary incontinence
Ataxia
Reduced cognition

Called ‘normal pressure’ as there is normal pressure on introduction of a spinal tap. There is still raised ICP, due to the accumulation of excess CSF within the ventricles.

Answer 78

A

Clinical presentation

General malaise
Fever
Reduced consciousness/cognition
Seizures
Meningism: Headache, photophobia, nausea/vomiting, neck stiffness, postive Kernig’s and Brudzinski’s sign
Signs of raised ICP and cranial nerve palsies
+/- rash
Children and babies: hypotonia, poor feeding, lethargy, hypothermia and bulging fontanelle

Typical rash of meningococcal septicaemia

Non-blanching, purpuric rash

Answer 79

A

Bacterial

Neisseria meningitidis: Gram negative diplococcus
Streptococcus pneumoniae: Gram positive (cocci/bacilli)

Viral (viral PCR should be performed on LP samples to determine the causative agent)

HSV
Enterovirus
VZV

Answer 80

A

Clinical features

Altered consciousness
Altered cognition
Unusual behaviour
Acute focal neurology
Acute onset focal seizures
Infectious prodrome: Fever, rash, lymphadenopathy, cold solds, conjunctivitis, meningeal symptoms

Common causes

Viral *most common*
- HSV, VZV, CMV, EBV, enterovirus, adenovirus, influenza virus
Bacterial
Fungal

Answer 81

A

Can present with rapidly deteriorating neurological function due to compression
Swinging fever
Back pain, with severe tenderness
Spinal root lesions

Key differential

Osteomyelitis

Answer 82

A

Aetiology

HSV, VZV and enterovirus are the most common causative agents

Diagnosis

Viral PCR of LP sample
Serum and

Management

Aciclovir may be provided by HSV or VZV viral meningitis
Tends to only require supportive care aside from this

Answer 83

A

Immunosuppression (iatrogenic, HIV/AIDS, post-transplant)
Multiple comorbidities
Recent contact with TB

TB usually spreads via blood-bourne spread to the brain following primary infection. Ziehl-Neelson staining may be used to identify TB (stains red on blue background)

Answer 84

A

Investigations

Blood cultures
CRP/ESR
FBC, U&Es, LFTs, clotting
VBG/ABG (lactate, glucose)
Viral serology
LP *check for raised ICP first*
- Viral PCR, MC&S, protein and glucose levels
- Send for CT is suspicious of raised ICP

Indication for LP

Suspected SAH, meningitis

Contraindications for LP

Infection at entry site
Clotting derangement
Raised ICP

Answer 85

A

Acute management in the community:

IM/IV benzylpenicillin

Secondary care management:

IV ceftriaxone (PLUS dexamethasone)

Exposure prophylaxis: Ciprofloxacin

Answer 86

A

For suspected HSV/VZV - aciclovir

Answer 87

A

Sensorineural hearing loss (use steroids to avoid this)
Seizures
Cognitive impairment
Memory loss

Answer 88

A

Synchronous electrical activity bilaterally distributed across both hemispheres. There are no localising features referable to a single hemisphere.

Tonic-clonic seizures: Loss of consciousness, limbs stiffen (tonic) and then jerk (clonic). May have one without the other. Post-ictal confusion and drowsiness
Myoclonic seizures: Sudden jerk of a limb, face or trunk. May be suddenly thrown to the ground or have a violently disobedient limb.
Atonic seizures: Sudden loss of muscle tone causing fall
Infantile spasms: Associated with tuberous sclerosis
Absence seizures

Answer 89

A

Syncope is a sudden, completely reversible loss of consciousness secondary to an acute reduction of cerebral perfusion, which may last from several seconds up to minutes.

Cardiac syncope: Arrhythomogenic, cardiovascular (structural outflow obstruction)
Reflex syncope: Vasovagal (pain, fear, injury, long periods standing, micturition, cough), carotid sinus syndrome, emotional syncope
Orthostatic syncope/postural hypotension

Non-syncopal events ddx: Seizure, vertebrobasilar insufficiency, hypglycaemia, craniocerebral injury, heatstroke, hyperventiliation

Investigations MUST include ECG, lying and standing BP, tilt table testing.

Answer 90

A

Differential diagnosis of epilepsy:

Provoked seizure (fatigue, hypoglycaemia, drug induced)
Raised ICP
Syncope (cardiac, vasovagal, orthostatic hypotension)
Stroke
Mechanical fall

Answer 91

A

Management:

Removal of nearby objects
Place blankets to lessen injury
Do not restrain

Drugs used:

Benzodiazepines: IV Lorazepam, buccal midazolam, PR diazepam
Can be repeated at 10 mins if no resolution
Phenytoin/sodium valporate/levetiracetam on admission

Answer 92

A

FBC: ?anaemia, ?infection
ECG: ?arrythmia, ?heart block
Lying and standing BP
Tilt table testing: ?orthostatic ?vasovagal
Carotid massage: ?carotid sinus sensitivity
Blood glucose
Carotid artery doppler
CT head

Answer 93

A

MUST inform the DVLA of your condition (online or via form):

Seizures when awake and affect consciousness: Can drive after 12 months seizure free
One off seizure when awake and lost consciousness: Reapply after 6 months
Only have seizures whilst asleep: Reapply after 12 months
Seizures which don’t affect consciousness or driving: Can reapply after 12 months
Bus coach or lorry:
- >1 seizure: 10 years without seizures or medications
- 1 seizure: 5 years without a seizure or medication
Insurance is not valid, could get a £1000 penalty, if they do not inform the DVLA obliged to break cnfidentiality and inform them

Answer 94

A

Pathological lesions: Demyelination of neurons

Common sites of involvement:

Optic nerve: Optic neuritis
Cerebellar peduncles: DANISH signs *consider how to elicit these signs*
Brainstem: diplopia (INO), facial weakness, hearing impairment, dysphagia, vertigo, bladder/bowel/sexual dysfunction
DCML and corticospinal tracts: UMN deficit, loss of vibration and proprioceptive sensation
Cognitive dysfunction

Answer 95

A

Gender: F>M

Age: 20 -45 years

Geographic: Northern areas ? link to Vitamin D

Associated with HLA-DR2 phenotype

Answer 96

A

Relapsing-remitting: Most common.

Primary progressive

Secondary progressive

Answer 97

A

Tend to come on over days to weeks, gradually resolve over weeks to months. Symptoms classically worse during a fever, hot weather or after exercise - as central conduction is slowed by increased body temperature (Uthoff’s phenomenon)

Clinical features:

Optic neuritis
Bladder/bowel/sexual dysfunction due to brainstem demyelination
Weakness/UMN signs due to corticospinal demyelination
Sensation changes (DCML - vibration, proprioception)

Answer 98

A

MRI: Plaques visible as hyperintensities in the brain and/or spinal cord

CSF analysis: Oligoclonal IgG bands seen

Metabolic panel: FBC, TSH, B12, folic acid, calcium, potassium

Visual evoked potentials: Prolonged conduction in occipital EEG reactions

Answer 99

A

Neurological:
- Stroke/TIA, GBS, SOL, CNS sarcoidosis, MND
Wilson’s disease (copper excess)
Metabolic
- Diabetic neuropathy
Autoimmune
- SLE with neurological involvement

Answer 100

A

Management of acute MS relapse

Steroids: Methylprednisolone IV OD for 3/7
Plasma exchange for severe or rapidly progressing disability

Long term management

Conservative management:
- Regular exercise
- Good sleep hygiene practices
- Smoking cessation
- Physio
Medical management:
- Disease modifying therapy for RRMS: Such as interferon beta

Answer 101

A

Rigidity (lead pipe)
Bradykinesia/ataxia
Tremor (resting)

Other features: Shuffling gait, serpentine stare, quiet and slow speech

Answer 102

A

Pathological basis: Degeneration of the dopaminergic neurons within the substantia nigra

Common clinical features:

Festinating/Parkinsonian gait: Slow, increasing turning circle, leaning forwards
Rigidity (lead pipe) with cogwheeling on passive movement
Ataxia
Bradykinesia: Asked to tap index finger to thumb sees slowing over time
Pill rolling, resting tremor: Unilateral, increased by distraction with opposite limb
Micrographia

Answer 103

A

Sleep disturbance: Excessive movement in sleep with acting out of dreams, insomnia in later disease
Mood: Depression
Cognition: Reduced in late stages of the disease
Anosia
Constipation, urinary frequency

Answer 104

A

Causes of Parkinsonism:

Medications: Prochlorperazine, neuroleptics (antipsychotics), metoclopramide, TCAs, methyldopa,
Vascular: Multiple cerebral infarcts
Toxin induced: Wilson’s disease
Parkinson’s plus syndromes: PSP, MSA, LBD, vascular Parkinsonism, cortico-basal degeneration