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Neurology Flashcards

1
Q

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

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2
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BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: Draw and label the circle of Willis and its branches

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3
Q

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

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4
Q

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

A

Cerebral hemisphere - Bulbar palsy, stroke/TIA

Brainstem - Pseudobulbar palsy

Cerebellum -

Basal ganglia - Parkinsonism and movement disorders

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5
Q

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

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6
Q

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

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

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7
Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: List the causes of dysarthria

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
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8
Q

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

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
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9
Q

BASIC NEUROANATOMY AND NEUROPHYSIOLOGY: List the causes of Horner syndrome

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
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10
Q

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

A

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

LMN: Forehead also affected

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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

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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

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)

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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

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
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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

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

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15
Q

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

A

Pt on side with knees fully flexed to the chest.

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

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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

A
  1. Lying on side with knees flexed to chest
  2. Sitting on the edge of the bed
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17
Q

LUMBAR PUNCTURE: List the potential complications of LP

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
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18
Q

LUMBAR PUNCTURE: List the contraindications to a lumbar puncture

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
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19
Q

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

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)
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20
Q

LUMBAR PUNCTURE: Explain the term CSF xanthochromia

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.

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21
Q

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

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).

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22
Q

LUMBAR PUNCTURE: List the CSF findings that accompany multiple sclerosis

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).
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23
Q

CT AND MRI: List the important contraindications to MRI

A
  • Metal implants or fragments
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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

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
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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

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
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26
Q

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

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.

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27
Q

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

A

Inspection

  • Reduced chest expansion

Auscultation

  • Reduced breath sounds

Investigations

  • Type 2 respiratory failure findings on ABG
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28
Q

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

A

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

Peak flow

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29
Q

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

A

Hypercapnia and hypoxia

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30
Q

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

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
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31
Q

HEAD INJURIES: List the features which reflect severe head injury

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

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32
Q

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

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
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33
Q

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

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
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34
Q

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

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)
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35
Q

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

A
  • Pneumocephalus from mask ventilation
  • Inadvertant placement of tubes within the cranium e.g. NG tubes
  • Carotid artery damage
  • Carotido-cavernous fistula
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36
Q

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

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)

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37
Q

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

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

​

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

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

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38
Q

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

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
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39
Q

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

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
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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

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

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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

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
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42
Q

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

A

Bedside: ECG,

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

Toxin screen (drugs and alcohol)

Imaging: CT/MRI head

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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.

A

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

  1. Suction
  2. Chin-lift manoeuvre
  3. Jaw thrust
  4. 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

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44
Q

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

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.

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45
Q

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

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

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46
Q

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

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.
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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

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

48
Q

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

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

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

A

Acute management of stroke

  1. 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,
  2. Once stroke is suspected administer 300mg aspirin
  3. CT head required to rule out haemorrhagic stroke
  4. Adminster thrombolysis if CT confirms ischaemic stroke AND symptom onset is within 4.5 hours
  5. Ongoing monitoring of patient vitals, with importance placed upon management of blood pressure, glycaemic control and temperature
  6. 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
50
Q

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

A
  • Assessment of swallow: Check swallow upon admission (cranial nerve assessment), SALT assessment should be performed
  • Rehabilitation
  • Nursing care
51
Q

CEREBROVASCULAR DISEASE: Outline measures undertaken in secondary prevention of stroke

A
  • Antiplatelet therapy: Clopidogrel 75mg OD
  • Antihypertensive
  • Statin
  • Anticoagulant if required (AF)
52
Q

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

A

Evaluating carotid stenosis

  • Auscultate for bruits
  • Carotid duplex scan

Managing carotid stenosis

  • Endarterectomy
  • Angioplasty and stenting
53
Q

CEREBROVASCULAR DISEASE: Outline medical and surgical management of TIA

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
    *
54
Q

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

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

55
Q

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

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.
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

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

57
Q

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

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
58
Q

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

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)

59
Q

SUBARACHNOID HAEMORRHAGE: Describe the acute management of SAH

A

Early management aims

  • Prevention of rebleeding
  • Prevention of delayed cerebral ischaemia due to vasospasm

Management

  1. Endovascular obliteration via platinum spirals (coiling) OR clipping to prevent rebleeding. Systolic BP should be kept < 180mmHg before.
  2. 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
  3. Supportive management:
    • Specialist referral - neurosurgery
    • Assessment of swallow
  4. Ventricular drainage if indicated (SAH complicated by hydrocephalus)
60
Q

SUBARACHNOID HAEMORRHAGE: List the potential complications of a subarachnoid haemorrhage

A
  • Rebleeding
  • Death ~30% die immediately
  • Vasospasm (leading to insufficient cerebral perfusion and can cause clot formation within vessels, ultimately causing obstruction)
  • Hydrocephalus
61
Q

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

A
  • Trauma (acceleration-deceleration injury)
  • Elderly
  • ETOH excess
  • Anticoagulant use
  • Clotting abnormalities (haemophilia)
62
Q

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

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
63
Q

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

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)
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

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

65
Q

INTRACEREBRAL HAEMORRHAGE: List the structural lesions and predisposing factors which may predispose towards deep intracerebral haemorrhage and lobar cerebral haemorrhage

A
  • Micro-aneurysms
  • Anticoagulants
  • Hypertension
66
Q

INTRACEREBRAL HAEMORRHAGE: Describe the clinical presentation of intracerebral haemorrhage, initial investigations and immediate patient management

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
67
Q

HEADACHE: Outline the features and management of headaches disorders including Tension Headaches, medication overuse headache, migraine, cluster headaches and giant cell/temporal arteritis

A
68
Q

HEADACHE: Describe features of the clinical presentation of a headache that might raise concern about a more sinister pathology, listing, in each case the relevant differentials and appropriate investigations

*think of ddx*

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

69
Q

TEMPORAL ARTERITIS: Describe the pertinent epidemiological features of temporal arteritis, including age at presentation and association with other inflammatory conditions

A

Epidemiology:

  • F>M
  • Patients > 50 years old

Associated conditions:

  • Polymyalgia rheumatica
  • Hip and shoulder girdle aching
  • Morning stiffness
70
Q

TEMPORAL ARTERITIS: Describe the pathologial process involved in temporal arteritis

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.

71
Q

TEMPORAL ARTERITIS: Describe the clinical features of a headache arising from temporal arteries and other associated symptoms and signs

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)
72
Q

TEMPORAL ARTERITIS: List the clinical investigations employed to confirm clinical suspicion of temporal arteritis

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 ↓
73
Q

TEMPORAL ARTERITIS: Describe the management of temporal arteritis

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).

74
Q

TEMPORAL ARTERITIS: Outline the main complication that arises from untreated or missed temporal arteritis

A
  • Bilateral visual loss
75
Q

RAISED INTRACRANIAL PRESSURE: List the main causes of raised ICP

A
  • Space occupying lesion
  • Intracranial haemorrhage (including stroke - intracerebral)
  • Hydrocephalus
  • Abscesses or infection: Meningitis
  • Idiopathic intracranial hypertension
76
Q

RAISED INTRACRANIAL PRESSURE: List the features in a headache which reflect a raised intracranial pressure

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
77
Q

RAISED INTRACRANIAL PRESSURE: List the pertinent examination findings in raised intracranial pressure

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
78
Q

RAISED INTRACRANIAL PRESSURE: List the potential complications of Acutely raised intracrianial pressure and Chronically raised intracranial pressure

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
79
Q

NEURO-ONCOLOGY: Describe the clinical presentation of an intracerebral space occupying lesion

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
80
Q

NEURO-ONCOLOGY: Explain the term paraneoplastic syndrome, and describe two paraneoplastic syndromes involving the nervous system

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.

  1. Myasthenia gravis - seen in thyoma and bronchogenic carcinoma
  2. Subacute cerebellar syndrome - ovarian cancer
  3. Paraneoplastic limbic encephalitis3
  4. Neuropathy2 - seen in lung, breast, myeloma, Hodgkin’s and GI
  5. 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

81
Q

NEURO-ONCOLOGY: List the three most common adult primary brain tumours and outline their prognosis

(name 4 - remember ‘subtypes’)

A

Glioma

  1. 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)
  2. Oligodendroglioma
  3. 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
82
Q

NEURO-ONCOLOGY: List the common somatic tumours which metastasise to the brain

A
  • Bronchus
  • Breast
  • Kidney
  • Colon
  • Thyroid
  • Malignant melanoma
83
Q

HYDROCEPHALUS: Describe the clinical triad reflective of normal pressure hydrocephalus

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.

84
Q

CNS INFECTION: Outline the clinical presentation of bacterial meningitis and describe the appearance of the typical rash of meningococcal septicaemia

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
85
Q

CNS INFECTION: Describe the common bacterial and viral organisms causing meningitis in adult life

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
86
Q

CNS INFECTION: Outline the clinical features of encephalitis and list the common causes

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
87
Q

CNS INFECTION: Describe the clinical presentation of an epidural spinal abscess

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

Key differential

  • Osteomyelitis
88
Q

CNS INFECTION: Describe the pathological changes and complications seen in purulent leptomeningitis, lymphocytic meningitis and granulomatous meningitis.

A

-

89
Q

CNS INFECTION: Discuss the aetiology, diagnosis and management of herpes simplex encephalitis.

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
90
Q

CNS INFECTION: List the risk factors which may predispose a patient to TB or fungal meningitis.

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)

91
Q

CNS INFECTION: Discuss the investigation of a patient with suspected meningitis including indications and contraindications for lumbar puncture.

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
92
Q

CNS INFECTION: Compare the CSF findings in bacterial, fungal and viral meningitis/encephalitis

A
93
Q

CNS INFECTION: Discuss an appropriate antibiotic regimen for treatment of bacterial meningitis

A

Acute management in the community:

  • IM/IV benzylpenicillin

Secondary care management:

  • IV ceftriaxone (PLUS dexamethasone)

Exposure prophylaxis: Ciprofloxacin

94
Q

CNS INFECTION: Suggest additional agents which may be added in Suspected viral meningoencephalitis

A

For suspected HSV/VZV - aciclovir

95
Q

CNS INFECTION: Outline the long-term complications of bacterial meningitis

A
  • Sensorineural hearing loss (use steroids to avoid this)
  • Seizures
  • Cognitive impairment
  • Memory loss
96
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Describe the classical features of a generalised seizure

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
97
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Outline the clinical types of syncope

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.

98
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Outline the features that distinguish seizures from syncope

A
99
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Outline a classification of epilepsy and describe the differential diagnosis of epilepsy

A

Differential diagnosis of epilepsy:

  • Provoked seizure (fatigue, hypoglycaemia, drug induced)
  • Raised ICP
  • Syncope (cardiac, vasovagal, orthostatic hypotension)
  • Stroke
  • Mechanical fall
100
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Outline the immediate ‘first aid’ treatment of a patient having a generalised seizure plus the drugs used to control an acute seizure

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
101
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Describe an investigation plan for a patient with recurrent syncope

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
102
Q

EPILEPSY & LOSS OF CONSCIOUSNESS (LOC): Describe the current laws dictating driving and epilepsy

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
103
Q

MULTIPLE SCLEROSIS: Describe the pathological lesions of multiple sclerosis, the common sites of involvement in the nervous system and outline the pathogenesis of the disease.

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
104
Q

MULTIPLE SCLEROSIS: Describe the epidemiological features of MS, with specific reference to gender, age of onset and geographic distribution

A

Gender: F>M

Age: 20 -45 years

Geographic: Northern areas ? link to Vitamin D

Associated with HLA-DR2 phenotype

105
Q

MULTIPLE SCLEROSIS: List the different clinical patterns of MS and describe the different courses that MS can take.

A

Relapsing-remitting: Most common.

Primary progressive

Secondary progressive

106
Q

MULTIPLE SCLEROSIS: Describe commonly encountered clinical features of MS relapses

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)
107
Q

MULTIPLE SCLEROSIS: List the investigations used in ascertaining a diagnosis in MS. Outline the diagnostic utility of magnetic resonance imaging (MRI), evoked potentials and CSF examination

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

108
Q

MULTIPLE SCLEROSIS: List the differential diagnosis of MS

A
  • Neurological:
    • Stroke/TIA, GBS, SOL, CNS sarcoidosis, MND
  • Wilson’s disease (copper excess)
  • Metabolic
    • Diabetic neuropathy
  • Autoimmune
    • SLE with neurological involvement
109
Q

MULTIPLE SCLEROSIS: Outline the management of MS (acute relapse and long term)

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
110
Q

MULTIPLE SCLEROSIS: Outline the principles of treatment of: immuno-suppression; symptomatic management and rehabilitation of spasticity, bladder problems, pain, sensory symptoms, weakness, fatigue and depression

A
111
Q

PARKINSON AND OTHER EXTRAPYRAMIDAL DISORDERS: Describe and recognise the clinical triad of Parkinsonism

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

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

112
Q

PARKINSON AND OTHER EXTRAPYRAMIDAL DISORDERS: Outline the pathological basis of classical Parkinson’s disease and describe the common clinical features

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
113
Q

PARKINSON AND OTHER EXTRAPYRAMIDAL DISORDERS: List non-motor features of Parkinson disease, with specific reference to disorders of sleep, mood and cognition

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
114
Q

PARKINSON AND OTHER EXTRAPYRAMIDAL DISORDERS: Outline less common causes of Parkinsonism including drugs and the Parkinson-plus syndromes

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
115
Q
A

CP3 (14 decks)

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