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J3 > Hersenen > Flashcards

Hersenen Flashcards

1
Q

Most common cause of radial nerve palsy

A

entrapment at spiral groove

‘Saturday night palsy’

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2
Q

presenting symptoms of radial nerve palsy

A
  • Wrist and finger drop
  • Usually painless
  • Motor weakness – mainly the extensors (wrist/finger extension)

Numbness over first dorsal interosseous muscle

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3
Q

Most common cause of ulnar nerve palsy

A

Entrapment at ulnar groove (medial epicondyle of humerus)

NB: Cyclists may end up with a problem due to excessive compression on the wrist

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4
Q

presenting symptoms of ulnar nerve palsy

A

May be history of trauma at elbow
• Sensory disturbance and weakness “weak grip”
• Usually painless
• Motor weakness - finger abduction/wrist flexion

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5
Q

Most common cause of median nerve palsy

A

entrapment within carpal tunnel at wrist
• Pregnancy
• hyperthyroisism

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6
Q

presenting symptoms of median nerve palsy

A

 History of intermittent nocturnal PAIN, numbness and tingling – often relieved by shaking hand
 Patient may complain of “weak grip”
 Positive Tinel’s sign/Phalen’s test (Wrist Flexion Test)
 Motor weakness

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7
Q

Most common cause of Anterior Interosseous Branch (median nerve) palsy

A

Trauma to forearm

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8
Q

presenting symptoms of Anterior Interosseous Branch (median nerve) palsy

A

unable to make ok sign
weak grip
history of trauma to forearm

no sensory changes

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9
Q

Most common cause of femoral nerve palsy

A

haemorrhage / trauma

May be iatrogenic (femoral lines)

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10
Q

presenting symptoms of femoral nerve palsy

A

 Not normally painful
 Weakness of Quadriceps = knee extension
 Weakness of Hip flexion/hip abduction
 Numbness in medial shin

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11
Q

Most common cause of common peroneal nerve palsy

A

entrapment at fibular head

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12
Q

Most common mononeuropathy in the lower limb

A

common peroneal nerve

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13
Q

presenting symptoms of common peroneal nerve palsy

A

May be history of trauma, surgery or external compression (crossing of legs)

 Acute onset foot drop + sensory disturbance
 Usually painless
 Motor weakness

NB: Foot drop is a common sign in neurology, but when it comes from Common peroneal nerve, ankle reflexes will be intact and foot inversion is still possible

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14
Q

Mononeuritis multiplex

A

painful, asymmetrical sensory and motor peripheral neuropathy

involves isolated damage to at least 2 separate nerves

causes tend to be systemic (DM, vasculitis, CT diseases, lymphoma, infection - Hep C/HIV)

Multiple nerves in random areas of the body can be affected.

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15
Q

What does breathlessness on lying flat indicate?

A

Weakness of the diaphragm

Worse on lying flat because the abdominal viscera exert pressure

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16
Q

Functions of the peripheral nervous system

A

sensory input to CNS
motor output to muscles
innervation of viscera

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17
Q

Causes of length-dependent axonal neuropathy

A

diabetes
alcohol

 Folate / B12 / thiamine /B6 deficiency
 RA, SLE, vasculitis
 Renal failure, hypothyroidism
 Drugs
 Infectious: HIV, hepatitis B & C
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18
Q

Guillain-Barré syndrome

A

Acute inflammatory demyelinating neuropathy

Progressive (ascending) weakness. Affects proximal muscles. +/- respiratory / bulbar / autonomic involvement

Flaccid, quadraparesis with areflexia

History of recent infection (campylobacter/EBV/CMV). Trigger infection causes formation of antibodies which attack the myelin sheath

Demyelination will cause conduction block

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19
Q

Myasthenia gravis

A

Autoimmune disorder: antibodies to nicotinic acteylcholine receptor at post-synaptic NMJ

May be associated with thymic hyperplasia or thymoma

Affects young women in 20’s and older men in 70’s

Fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles

Antibodies to AChR present in 85% of cases

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20
Q

commonest type of peripheral neuropathy

A

Length-dependent axonal neuropathy

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21
Q

Which condition presents with ascending flaccid tetraparesis?

A

Guillain-Barré syndrome

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22
Q

Which condition is characterised by formation of antibodies against post-synaptic acetylcholine receptor?

A

Myasthenia gravis

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23
Q

Primary headache vs Secondary headache

A

Primary headache = headache and its associated features is the disorder (no underlying cause)
• E.g. Migraine, tension-type headache, cluster headache

Secondary headache = secondary to underlying cause
• E.g. Subarachnoid haemorrhage, SOL, meningitis, temporal arteritis, high/low ICP, drug-induced

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24
Q

‘Red Flag’ features suggesting secondary headache

A

= SNOOPT
 Systemic symptoms
 Neurological signs or symptoms (focal/non-focal)
 Older age at onset (>50)
 Onset is acute (under 5 minutes) = thunderclap
 Previous headache history is different / absent
 Triggered headache (valsalva or posture)

Assess cranial nerves and fundoscopy

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25
Q

Aura

A

Recurrent reversible focal neurological symptom (eg. visual, sensory, motor)

Develops over 5-20 mins and lasts <60 mins

Visual aura is most common (eg. scotoma, flashing lights, fortification spectrum)

Sensory aura often starts in hand and migrates up arm

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26
Q

Migraine presentation

A 
Headache:
• commonly throbbing or pulsatile
• Moderate – severe intensity
• Gradual onset, duration 4 –72hrs
• Unilateral in 60%, can radiate
• Aggravated by routine physical activity
Associated symptoms
• Nausea and vomiting
• Photophobia
• Phonophobia
• Osmophobia
• Mood disturbance
• Diarrhoea
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27
Q

Medication overuse headache

A

headache 15+ days per month associated with frequent

use of acute relief medications

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28
Q

Management of migraine

A
  • Avoid triggers
  • Reduce caffeine / alcohol intake
  • regular meals and sleep patterns

Acute management
• Simple analgesia (Paracetamol, Aspirin, NSAIDs)
• Triptans (eg. Sumatriptan)
• +/- antiemetic (eg. domperidone, metoclopramide)

Prophylaxis
• Beta-blockers (Propanolol)
• Tricyclic antidepressants (Amitriptyline, Nortriptline)
• Anti-epilepsy drugs (Sodium Valproate)

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29
Q

Thunderclap headache

A

abrupt-onset of severe headache which reaches maximal intensity <5 mins (and lasts >1 hr)

“worst headache of life”
“like being hit over the head”

considered as SAH until proven otherwise

Other causes:
• Intracerebral haemorrhage
• Arterial dissection (vertebral or carotid)
• Cerebral venous sinus thrombosis
• Bacterial meningitis
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30
Q

Investigation of thunderclap headache

A

Aim to identify SAH

Bloods
ECG
CT brain
LP - Performed after 12 hours to look for xanthochromia
Intracranial pressure
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31
Q

xanthochromia

A

yellow discoloration indicating the presence of bilirubin in the cerebrospinal fluid

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32
Q

Raised pressure headaches: features

A

Worse on lying flat, improved on sitting / standing up

Worse in the morning

Persistent nausea / vomiting

Worse on valsalva (eg. coughing, laughing, straining)

Worse with physical exertion

Transient visual obscurations with change in posture

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33
Q

Raised pressure headaches: examination findings

A

Optic disc swelling – papilloedema

Impaired visual acuity / colour vision

Restricted visual fields / enlarged blind spot

III nerve palsy

VI nerve palsy (false localizing sign)

Focal neurological signs

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34
Q

Causes of raised ICP

A

Mass effect - tumour, oedema, haematoma, abscess

Increased venous pressure - cerebral venous sinus thrombosis, obstruction of jugular venous system

Obstruction to CSF flow / absorption - hydrocephalus, meningitis

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35
Q

Low CSF pressure headache features

A

Headache worse on sitting / standing up and relieved by lying down

Loss of CSF volume causes traction on meninges, cerebral / cerebellar veins and CN V, IX and X

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36
Q

Causes of Low CSF pressure

A

Post-lumbar puncture

Spontaneous intracranial hypotension due to dural tear

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37
Q

Stroke

A

Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more
than 24 hours or leading to death, with no apparent cause other than that of vascular origin.

objective evidence of focal ischaemic injury in a defined vascular distribution

Anything <24 hours is classified as a TIA

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38
Q

Stroke pathophysiology

A

Always due to a blood clot somewhere, e.g. heart/venous system

Blood clot ascends to the brain through the blood vessels

Blood flow is stopped, and brain becomes starved of oxygen

Neurons are depolarized

Early symptoms -> loss of function. If blood flow is restored at this point, the damage is reversible

Brain tissue dies causing areas of infarction. This is irreversible damage

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39
Q

Acute signs/symptoms of stroke

A

Unilateral weakness: leg/ face & arm/ hemiparesis. body parts affected indicate the location of the lesion due to the differential relative representation on the
motor/somatosensory cortices

Dysphasia

Visual disturbance: e.g. right homonymous heminopia

Acute light-headedness (past-pointing, nystagmus)

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40
Q

A stroke can cause expressive or receptive aphasia. Which artery is most likely the blocked one? And which side of the body will likely show motor signs of stroke?

A

Left MCA

Broca’s/Wernicke’s are located in the left hemisphere in the majority of people.

Right side of the body will be affected (left motor cortex controls the right side of the body)

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41
Q

Definition of ischaemic stroke

A

An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction.

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42
Q

Causes of ischaemic stroke

A

Cardiac embolism – e.g. AF, heart failure

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43
Q

Total Anterior Circulation Syndrome (TACS)

A

Hemiparesis + Higher cortical dysfunction + hemianopia

Usually proximal MCA or ICA occlusion

Remember: 3H’s

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44
Q

Partial Anterior Circulation Syndrome (PACS)

A

o Isolated higher cortical dysfunction OR
o Any 2 of hemiparesis, higher cortical dysfunction, hemianopia

Usually branch MCA occlusion

Remember: Partial, therefore only part (2/3Hs)

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45
Q

Posterior Circulation Syndrome (POCS)

A

Isolated hemianopia OR Brainstem syndrome

Can include perforating arteries, PCA or cerebellar arteries

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46
Q

Lacunar Syndrome (LACS)

A 
Pure motor stroke 
OR pure sensory stroke 
OR sensorimotor stroke 
OR ataxic hemiparesis
OR clumsy hand-dysarthria

Small vessel disease (deep perforating vasculopathy)

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47
Q

Definition of intracerebral haemorrhage

A

A focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma.

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48
Q

Patient presents with new onset expressive dysphasia which he woke up with. What kind of stroke is this?

A

PACS

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49
Q

Patient presents with sudden onset speech disturbance and left-sided weakness 1 hour ago.

O/E: left hemiparesis, left sided hemianopia, left sided neglect

What kind of stroke is this?

A

TACS

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50
Q

Patient presents with sudden onset right sided weakness 5 hours ago.

O/E: hypoasthaesia right face, arm, leg. No movement against gravity in right arm and leg.

What kind of stroke is this?

A

LACS

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51
Q

Patient presents with left sided neck pain since skiing 2/7 ago. Sudden onset vertigo and ataxia yesterday.

O/E: nystagmus, right ptosis, small pupil on right, hypoasthaesia right face, arm, leg, hoarse, right upper limb ataxia

A

POCS

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52
Q

Treatment approach: Ischaemic stroke

A

IV thrombolysis +/- thrombectomy. Aspirin

Thrombolysis must be within 4.5 hours of onset
Thrombectomy within 6-8 hours. For large vessel disease only

Stroke unit care -> coordinated care, short/long term therapy, prevent aspiration

Hemicranectomy

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53
Q

Treatment approach: Haemorrhagic stroke

A

Intracerebral bleed requires aggressive control of blood pressure

Stroke unit care -> coordinated care, short/long term therapy, prevent aspiration

Neurosurgical evaluation

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54
Q

GCS: Eye Opening

A

4 - Spontaneous
3 - to verbal command
2 - to pain
1 – none

N.B. cannot be assessed if eyes are swollen

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55
Q

GCS: Verbal Response

A 
5–oriented (T/P/P)
4–confused
3–inappropriate
2–incomprehensible sounds
1–none

NB. Append “T” to score if patient is intubate

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56
Q

GCS: Motor

A 
6 - Obeys commands
5 - Localizes pain
4 - Normal Flexion
3 - Abnormal flexion – looks robotic, slow and unnatural (decorticate)
2 - Extension (decerebrate)
1 – None
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57
Q

Coma according to GCS

A

Coma = inability to:
o Obey commands
o Speak
o Open eyes to pain

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58
Q

Classification of head injury using GCS

A 
Minor = 14-15
Moderate = 9-13
Severe = <8

Significance:
consistent strong association between motor score and 6-month Glasgow Outcome Scale (GOS)

GCS and 14-day mortality is ~linear
GCS and 6-month poor outcome is ~linear

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59
Q

Most common cause of SAH

A

trauma

NB: with spontaneous SAH 80-85% are caused by aneurysms.

o 15-20% non-aneurysmal
 Tumours
 Arteriovenous malformations
 Anticoagulant therapy

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60
Q

Aneurysmal SAH - Predisposing factors

A 
 Smoking
 Female sex
 Hypertension
 Positive family history
 ADPCK, Ehlers Danlos, coarctation of the aorta
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61
Q

SAH History

A 
 Sudden onset (thunderclap) headache
 LOC
 Seizures
 Visual disturbance
 speech and limb disturbance
 Sentinel headache in 30%
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62
Q

Clinical examination findings with SAH

A 
 Photophobia
 Meningism - Nuchal rigidity (irritation of the dura)
 can present with CHF/pulmonary oedema
 Subhyaloid hemorrhages 
 Vitreous haemorrhages 
 Speech and limb disturbance
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63
Q

WFNS grading of SAH

A 
 Grade I - GCS 15
 Grade II - GCS 13-14 without deficit
 Grade III - GCS 13-14 with deficit
 Grade IV - GCS 7-12
 Grade V - GCS 3-6

Higher grade = more severe and worse prognosis

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64
Q

Investigation- SAH

A

CT confirms diagnosis and identifies complications

LP: xanthochromia - bilirubin (Takes 6-8 hours post SAH to produce)

If unclear, perform invasive imaging (CTA/DSA)

NB: there may be nonspecific ECG changes and slightly elevated troponin

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65
Q

complications of SAH

A

1) Rehaemorrhage - most common in first 72h
2) Hydrocephalus - due to obstruction of CSF flow
3) Delayed ischaemia - d3-10, due to vasospasm. Give nimodipine
4) Hyponatraemia
5) Cardiopulmonary complications - catecholamine release can lead to myocardial injury (“Stunned Myocardium”)
6) Seizure
7) DVT

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66
Q

SAH management

A

Conservative:

  • analgesia
  • fluid resuscitation
  • nimodipine to prevent Ca dumping and protect against delayed ischaemia
  • Anti-embolic stockings due to DVT risk

Surgical

  • clipping
  • Endovascular stents
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67
Q

Seizure

A

Episode of neuronal hyperactivity causing symptoms and signs (can be localized or can spread)

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68
Q

Epilepsy

A

A syndrome – spectrum of diseases

Characterized by a tendency to have unprovoked seizures

At least two unprovoked episodes of seizure (i.e. it’s not epilepsy if they have seizures following head injury)

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69
Q

Focal epilepsy

A

= partial

An area of abnormality in an otherwise normal brain

Causes irritability, causing hypersynchronous discharge,

focal epilepsy can cause either focal or generalized seizures

70
Q

Generalised epilepsy

A

a generalized tendency towards repeated APs and discharge

usually due to genetic causes - disorder of ion channels/metabolism of neurotransmitters

affects the whole brain at once, causing generalized seizures

71
Q

Focal Epilepsy Features

A

History of trauma / (ischaemic) birth injury

Focal aura / sequelae

Automatisms

Nocturnal events

Worse post-attack confusion / drowsiness

72
Q

Genetic Generalised Epilepsy (GGE) Features

A

Photosensitivity

Age of onset = 8-26

Alcohol or sleep deprivation

Myoclonus

Lack of aura (aura = specific area of discharge)

Seizures within 2 hours of awakening - Likely to happen early in the day because GGE is not focal, and therefore there is no build up

Family History in 30%

EEG abnormal

73
Q

Differential diagnosis for first seizure

A 
o syncope
o Migraine
o Narcolepsy / cataplexy
o Transient Global Amnesia
o Panic attacks
74
Q

Status Epilepticus

A

> 2 seizures without full recovery of neurologic function between seizures

Or continuous seizure activity >30 mins

75
Q

Treatment of focal epilepsy

A

o Carbamazepine
o Lamotrigine
o Levetiracetam

76
Q

Treatment of generalised epilepsy

A

o Valproate
o Lamotrigine
o Levetiracetam

77
Q

Multiple Sclerosis

A

Idiopathic Inflammatory Demyelinating Disease of CNS

results in the destruction of myelin in brain/spinal cord

Acute episodes of inflammation are associated with focal neurological deficits
• usually develop gradually
• last for more than 24 hours
• may gradually improve over days to week

78
Q

Subtypes of MS

A

Relapsing remitting Multiple Sclerosis
• Most common form
• Attacks initially come and go
• Can develop into secondary progressive MS

Primary Progressive Multiple Sclerosis
• At least 1 year of disease progression
• Gets worse without relapses

Secondary progressive Multiple Sclerosis
• RRMS in past but now progressive disease without relapses

Benign Multiple Sclerosis

79
Q

Syndromes that may develop into MS

A

1) optic neuritis = inflammation of optic nerve. Causes painful visual loss
2) transverse myelitis = inflammation of spinal cord
3) clinically isolated syndrome = single episode of neurological disability due to focal CNS inflammation
4) radiologically isolated syndrome

80
Q

Multiple sclerosis diagnosis requirements

A

2 or more episodes of demylination disseminated in space and time

Presence of oligoclonal bands in spinal fluid counts as evidence of dissemination in space and time

NB: It is possible to make the diagnosis of MS with one scan. Evidence of demylination in 2 regions can indicate dissemination in space. If enhancing and non-enhancing areas of demyelination are seen this can indicate dissemination in time (old and new lesions)

81
Q

Causes of MS

A

unknown - multifactorial

Genetic Factors – there are about 200 risk genes (e.g. vitamin D metabolism genes)
Sunlight/vitamin D exposure
Viral trigger - possibly EBV
Smoking

82
Q

investigation of suspected MS

A

MRI brain and cervical spine with gadolinium contrast

LP with matched blood sample to look for oligoclonal bands. Bands in CNS only indicated antibody production in CNS

Bloods to rule out differentials - B12/lyme/ANA/ANCA/RF

Visual evoked potentials to detect subclinical optic neuritis

CXR - exclude sarcoidosis

83
Q

MS Relapse Vs. Pseudo-relapse

A

A relapse usually involves a new neurological deficit that lasts for more than 24 hours in the absence
of pyrexia or infection

A pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old
area of demylination in the context of heat or infection

84
Q

MS treatment

A

Treat some relapses with steroids, but this does not affect disease progression, so it’s important to weigh up risks/benefits

No licensed DMARD. Some available but bad secondary immune consequences

Biotin supplement may give some symptom relief - gives energy to damaged nerve cells

Mainstay is symptom management

85
Q

Describe the spinal reflex arc

A

Ia fibre from muscle spindle senses stretching of a muscle

It synapses directly onto two neurons in the anterior horn:
1) an alpha motor neuron - excites the muscle group causing contraction

2) an inhibitory interneuron -> inhibits the antagonist muscle group

86
Q

Parkinson’s disease

A

Slowly progressing neurodegenerative disorder

Loss of dopaminergic neurons within substantia nigra

Surviving neurons contain Lewy bodies = misfolded protein within the cytoplasm of the cell (neurotoxic)

87
Q

Clinical features – parkinsonism

A

Remember: Facial TRAPS

Facial = expressionless face

T= tremor (pill-rolling) - predominantly at rest.

R= rigidity (cog-wheel)

A= akinesia. NB: Bradykinesia has two components:
• slowness in initiation of voluntary movement
• progressive reduction in speed and amplitude of repetitive actions

P= posture stooped - due to loss of the reflexes that keep you upright

S=shuffling gait

NB: Asymmetric disorder. Starts and remains worse on one side

88
Q

Non-motor symptoms of PD

A

Neuropsychiatric:
• Dementia
• Depression
• Anxiety

REM sleep behaviour disorder

Autonomic dysfunction

89
Q

Differential diagnosis of PD

A

Benign tremor disorders (e.g. essential tremor)
Dementia with Lewy bodies
Vascular parkinsonism
Parkinson plus disorders
Drug-induced parkinsonism/tremor (antipsychotics)

90
Q

Investigation of PD

A

Diagnosis of PD is largely clinical diagnosis

Bloods to rule out other causes of tremor

CT / MRI brain tends to be normal in PD

Imaging of presynaptic dopaminergic function using DATSPECT => shows loss of DA neurons

91
Q

Drug treatment of PD

A
  • L-dopa
  • Dopamine agonists
  • MAO-B inhibitors
  • COMT- inhibitors
92
Q

L-dopa

A

Taken up by dopaminergic neurons and decarboxylated to dopamine within presynaptic terminals

Prescribed with dopa-decarboxylase inhibitor

Approx. 50% of patients develop motor complications after 5 years(carbidopa)

93
Q

Dopamine agonists

A

 Ropinirole
 Pramipexole
 Rotigotine
 Apomorphine

Act directly on post-synaptic dopamine receptors (D2)

Increase sensitivity to endogenous dopamine

fewer motor complications than L-dopa

Can cause impulse control disorders (eg. Pathological
gambling, hypersexuality)

94
Q

MAO-B inhibitors

A

Eg. Selegiline, Rasagiline

Prevents dopamine breakdown by binding irreversibly to monoamine oxidase

Can be prescribed as monotherapy in early disease or as adjunct in later disease

95
Q

COMT inhibitors

A

Eg. Entacapone, Tolcapone

Inhibiting Catechol-o-methyltransferase results in longer L-dopa half-life / duration of action

Co-prescribed with L-dopa in later disease

96
Q

Nonpharmacological options for PD

A

Deep brain stimulation of subthalamic nucleus

Treatment option in advanced disease

Surgical implantation of electrodes to stimulate subthalamic nucleus

97
Q

Definition - dementia

A

Syndrome of progressive global decline in cognitive function

Interferes with the ability to function at work or at usual activities

Represents a decline from previous levels of functioning and performing

Is not explained by delirium or major psychiatric disorder

Severe, acquired and must involve more than one brain region

98
Q

Cognitive History

A

Remember: MEAL

 Memory
o repetitive questions or conversations
o misplacing personal belongings
o forgetting events or appointments
o getting lost on a familiar route

 Executive function
o poor understanding of safety risks
o inability to manage finances
o poor decision-making ability

 Apraxia/ Visuospatial
o inability to recognize faces or common objects
o Inability to find objects in direct view despite good acuity

 Language
o difficulty thinking of common words while speaking
o hesitations
o speech, spelling, and writing errors

99
Q

MMSE pros/cons

A

quick and easy
high interrater reliability

insensitive to early impairments
poorly covers executive function
influenced by age/education/SE status

100
Q

Addenbrookes Cognitive assessment pros/cons

A

More sensitive than MMSE in early disease
covers executive function
more detailed assessment

time consuming

101
Q

Alzheimer’s pathology

A

 Early loss episodic memory = Alzheimer’s disease
 Classically starts in temporal lobe
 Spreads to parietal and frontal lobes

Logopenic variant aphasia- Impaired single word retrieval

102
Q

Semantic Dementia

A

type of FTD

characterised by inability to match certain words with their images or meanings

Loss of knowledge about the world including words

103
Q

What type of dementia causes loss of episodic memory?

A

AD

104
Q

What type of dementia causes loss of semantic memory?

A

Semantic Dementia

105
Q

What defect causes impaired attention/concentration?

A

delirium

106
Q

Pupillary Light reflex

A

Afferent pathway:

  1. Action potential generated in optic nerve
  2. Axons synapse at right and left pretectal nuclei

Efferent pathway:

  1. AP passes to right and left Edinger-westphal nuclei
  2. AP conducted along both oculomotor nerves
  3. Constriction of:
     Pupil being illuminated = direct reflex
     Contra lateral pupil = consensual reflex
107
Q

What can cause a Relative Afferent Pupil Defect (RAPD)?

A

Disease of optic nerve or retina
o E.g. optic neuritis
o Large retinal detachment

Affected eye will initially paradoxically dilate in response to the light

108
Q

How would you demonstrate unilateral optic nerve lesion?

A

Swinging flashlight test

109
Q

ACCOMMODATION CONVERGENCE RELFEX

A

Pupil constricts to see distant object and get light rays parallel

Lens accommodation

Convergence of the eyes (contraction of both medial rectus muscles)

110
Q

Meningitis

A

Inflammation of meninges +/- cerebrum (meningo-encephalitis)

Can be acute or subacute

Can be bacterial or viral. Higher mortality associated with bacterial

111
Q

what are the characteristics of inflammatory CSF?

A

 High WCC
 Low glucose compared to blood glucose
 High protein count

May be bacterial but patient has had antibiotics, therefore the CSF is sterile

NB: glucose levels will be normal in viral meningitis

112
Q

Meningitis Symptoms and Signs

A 
95% will have 2 of:
o Headache
o neck stiffness (only 50%)-> late symptom!
o reduced GCS
o fever

 Confusion is indicative of cerebritis/encephalitis
 Rash – purpuric +/or petechial but macular early on (meningococcal disease)

113
Q

pneumococcus appearance

A

gram positive diplococcus

remember: Pneumococcus is Positive

114
Q

meningococcus appearance

A

Gram negative diplococci

115
Q

Risk factors for PNEUMOCOCCAL CNS infection

A 
70% underlying disorder:
 Middle ear disease
 Head injury (CSF leak)
 Neurosurgery
 Alcohol
 Immunosupression (HIV)
116
Q

Risk factors for Listeria CNS infection

A

 Transmitted through eating unpasteurised foods, e.g. cheese/pate
 Immunosupression
 Pregnancy
 Listeria causes a subacute meningoencephalitis

117
Q

Pneumococcal Meningitis

A

focal signs
seizures
VIII palsy

Other signs of Pneumococcal infection:
o CAP
o ENT
o Endocarditis

Bad prognostic outcome

118
Q

Meningococcal meningitis

A

characteristic rash

medical emergency

119
Q

When to do a CT (in suspected meningitis)

A 
CT before LP if there are signs of raised ICP:
o GCS ≤ 12
o CNS Signs
o Papilloedema
o Immunocompromised
o Seizure

Always give ANTIBIOTICS PRE-CT SCAN

120
Q

Treatment of suspected bacterial meningitis

A

Do not delay starting IV Antibiotics

Treat for Meningococcus/Pneumococcus and HI
- Ceftriaxone penetrates CNS well

If ≥ 60yrs/risk factors for Listeria add IV amoxicillin

If there is a high likelihood of Pneumococcus add steroids (dexamethasone)

121
Q

Meningococcal (secondary) Prevention

A

Give close contacts secondary prophylaxis

Chemoprophylaxis (Ciprofloxacin or Rifampicin)

knock out the carrier

122
Q

what kind of meningitis are patients with cochlear implants most susceptible to?

A

pneumococcal

123
Q

Most common cause of Viral Meningitis

A

enterovirus

124
Q

Management of Viral Meningitis

A

supportive treatment

Consider acyclovir ONLY if immunocompromised

125
Q

Intra-cerebral TB

A

Sub-acute (weeks)

CN lesions usual (III, IV, VI, IX)

Require steroids to reduce inflammatory response

Paradoxical worsening usual

126
Q

HIV Brain disease

A

Consequence of unrecognised/untreated infection and marked immunodeficiency

127
Q

Cryptococcal meningitis

A 
seen in immunodeficiency (HIV)
Raised ICP (often require a shunt)

May develop blindness and pulmonary/cutaneous lesions

CSF examination:
o India ink
o Cryptococcal antigen (also blood)
o Culture

128
Q

Causes of bacterial meningitis

A

meningococcus
pneumococcus
haemophilus influenza
TB

129
Q

Which artery supplies areas of the brain associated with speech?

A

MCA

130
Q

Transient ischaemic attack (TIA)

A 
brief episode (<24h) of neurological dysfunction due to a temporary focal cerebral/retinal ischaemia
without infarction

e.g. a weak limb, aphasia or
loss of vision, usually lasting seconds or minutes
with complete recovery.

131
Q

What is the most common type of stroke?

A

Ischaemic stroke (85%)

Usually caused by thromboembolic disease secondary to atherosclerosis.

Usually a problem with the anterior (carotid) circulation = TACS/PACS/LACS

Posterios circulation (vertebrobasilar arteries) causes POCS

132
Q

Haemorrhagic Stroke subtypes

A

Intracerebral haemorrhage
Subarachnoid haemorrhage

either a brain aneurysm burst or a weakened blood vessel leak. Blood spills into or around the brain and creates swelling and pressure, damaging cells and tissue in the brain.

133
Q

Most common site of a berry aneurysm

A

Anterior communicating artery

134
Q

“bulbar weakness”

A

= weakness of the cranial nerves from the medulla

cranial nerves 9, 10, 11, 12

Gives rise to dysarthria (difficulty speaking) and dysphagia because they supply muscles of the oropharynx

135
Q

What is the natural direction of the eyes?

A

The orbits naturally point the eyes laterally and superiorly

136
Q

Diplopia

A

Patient will complain of diplopia (double vision) if one of the cranial nerves isn’t working

Diplopia is worsened by looking in the direction of action of the muscle innervated by that nerve

137
Q

Abducens nerve palsy

A

prevents the affected eyeball from moving laterally beyond the midpoint
 The eyeball usually is directed medially.
 This leads to strabismus (crossed eyes) and diplopia.

Can be a nonspecific sign of raised ICP (forced localizing sign)

Images become separated horizontally

138
Q

Internuclear ophthalmoplegia (INO)

A

Midbrain lesion

Commonly seen in multiple sclerosis

causes failure of adduction of affected eye and nystagmus in the contralateral eye (only during
abduction)

139
Q

Herpes zoster ophthalmicus

A
  • Affects CN V1 division
  • Pain may precede vesicles
  • Elderly and immuno-compromised at risk
  • Treated with oral aciclovir
140
Q

How can you distinguish clinically between a LMN cause and UMN cause of the facial palsy?

A

a patient withforehead sparing(i.e. no involvement to the occipitofrontalis muscle) will have a UMN origin to
the palsy, due to the bilateral innervation of the forehead muscle).

LMN will affect the entire half of affected side of face

141
Q

hypoglossal palsy

A

Muscles push the tongue out, so if they are not functioning, the tongue deviates towards the sign of the lesion

142
Q

ROSIER score

A

used to distinguish between suspected stroke and stroke mimics

143
Q

Stroke Ddx

A 
 Head injury
 Hypoglycaemia
 Subdural haemorrhage
 Intracranial tumour
 Hemiplegic migraine
144
Q

Causes of haemorrhagic stroke

A

o CNS bleeds from trauma

o Ruptured aneurysm

145
Q

Causes of ischaemic stroke

A

o Small vessel occlusion
o Atherothromboembolism
o Cardiac emboli
o Emboli secondary to AF

146
Q

Which tests would you request in a suspected stroke?

A 
Bloods to check fitness for thrombolysis:
FBC -> platelet count crucial
U&amp;Es
CRP/ESR
LFTs
Coagulation profile

Glucose -> exclude hypoglycaemia
Lipid profile -> assess risk

CT brain
ECG - to look for ischaemic changes or rhythm abnormalities e.g. AF

CT angiogram to identify the site of occlusion

147
Q

What is the role of imaging in acute stroke?

A

 Exclude mimics (tumours, subdural haematoma)

 Distinguish ischaemic from haemorrhagic stroke
o Used to rule out a bleed

 Identify site of thrombus (CTa and MRa)

148
Q

ischaemic penumbra

A

MRI

region with reduced blood flow (seen on perfusion scan) but no lesion on diffusion weighted imaging (DWI)

presumed to be ‘at risk’ but ‘potentially salvageable’

149
Q

What kind of stroke would proximal occlusion of the left MCA cause?

A

TACS

150
Q

Which drug is used for intra-venous thrombolysis (IVT)?

A

Alteplase

151
Q

Mechanisms of Cell Death after Stroke.

A

Initial ischaemia (reversible) followed by infarction (irreversible damage)

1) excitotoxity
2) peri-infarct depolarization
3) oxidative stress
4) inflammation
5) apoptosis

152
Q

Secondary stroke prevention

A

A - antiplatelet -> aspirin + clopidrogrel

B - BP control -> ACEi + thiazide diuretic

C - cholesterol -> statin

D - diabetes control

depending on patient deficit:
 Physiotherapy
 Speech therapy/swallowing assessment
 Occupational therapy
 Smoking cessation
 Dietician
153
Q

A patient who is on secondary stroke prevention medication has AF. What do you do?

A

Assess need for anticoagulant therapy using CHA2DS2VASC score. Give therapy to scores of 2+

use HAS-BLED score to calculate risk of major bleed.

STOP ANTI-PLATELET THERAPY if you give anticoagulant

154
Q

incidence, prevalence and economic burden of stroke

A

 commonest neurological disorder and cause of disability worldwide.

 accounts for 1 in 18 deaths in western countries.

 3rd most common cause of death

 consumes 5% of the entire NHS budget

155
Q

Stroke signs and symptoms

A

sudden onset focal CNS signs

Facial asymmetry

Arm/leg weakness (contralateral hemiparesis)

Speech difficulty - slurred, aphasia/dysphasia

Visuospatial neglect

Contralateral homonymous hemianopia

156
Q

Uhthoff’s phenomenon

A 
o Heat (exercise) causes worsening of nerve function
o This is seen in demyelination.
157
Q

optic neuritis presentation

A

pain on eye movement and visual blurring associated with rapidly decreased central vision

can manifest as red desaturation.

158
Q

Outline a strategy for the diagnosis of MS

A

clinical diagnosis based on clinical history supported by examination findings and investigation results.

Exclude mimics (bloods and MRI brain + spinal cord)

Supporting investigations:
 MRI findings
 LP -> inflammation in CSF (positive oligoclonal bands)
 other evidence which may represent demyelination such as abnormal visual evoked responses
(VERS).

The diagnosis of MS is made when we demonstrate two neurological lesions are disseminated in space
and time.

159
Q

MS Ddx

A

sarcoidosis

Lyme disease

B12 deficiency

vasculitis

160
Q

What are VERS?

A

Visual evoked responses

measure the speed at which impulses travel along the optic nerve.

161
Q

What form of imaging would you use to show demyelination?

A

Demyelination shows up as white lesions on T2 MRI

162
Q

What treatment options exist in progressive MS?

A

Treatment options in progressive MS are directed at symptom control.

There is currently no way of reversing damage to the nervous system or stopping progressive disease.

163
Q

clinical features of raised intracranial pressure:

A

 Papilloedema

 Constriction of visual fields;

 Enlargement of the blind spots;

 VIth nerve palsy - may be a false localising sign

reduced GCS
Pain

164
Q

What investigations would you perform for suspected migraine?

A

Blood tests

Neuroimaging - Not indicated. may demonstrate incidental abnormalities -> unnecessary anxiety

165
Q

Migraine Ddx

A

tension-type headache

trigeminal autonomic cephalgias (eg cluster headache).

tension-type headache is usually featureless (no nausea, not aggravated by physical activity)

trigeminal autonomic cephalgias are unilateral and associated with prominent ipsilateral cranial autonomic features.

166
Q

Discuss the pathogenesis of migraine

A

considered a neurovascular disorder.

probably dysfunction in sensory brainstem nuclei.

pain results from interactions between components of the trigeminovascular system:

  1. The pain-sensitive cranial blood vessels;
  2. The trigeminal nerve fibres that innervate them; and
  3. The cranial parasympathetic outflow.

aura phase is associated with reduction of blood flow in contralateral hemispheric regions

167
Q

differential diagnosis for thunderclap headache

A 
 SAH;
 Intercerebral haemorrhage;
 Cerebral venous sinus thrombosis;
 Arterial dissection (vertebral or carotid);
 Bacterial meninigitis;
168
Q

risk factors for subarachnoid haemorrhage

A

Modifiable:
o smoking
o hypertension
o alcohol excess

Non-modifiable:
o previous SAH
o polycystic kidney disease
o connection tissue disease (Ehler’s Danlos, Marfan)
o arteriovenous malformations
o strong family history (>2 first-degree relatives)

169
Q

‘surgical’ IIIrd nerve palsy.

A

IIIrd nerve palsy with dilatation of the pupil

This is because the parasympathetic fibres that supply pupillary constrictor muscles run along the outside of the IIIrd nerve and are subject to compression from ‘surgical’ causes (eg tumour or aneurysm).

170
Q

isolated, complete IIIrd nerve palsy with dilatation of the pupil

A

due to an aneurysm of the posterior communicating artery until proven otherwise.

J3 (18 decks)

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