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Year 4 > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

Where is CSF produced? How much/day

A

From arterial blood in the choroid plexus of the lateral and 4th ventricles
Diffusion, pinocytosis and active transport
600ml/day

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2
Q

How much CSF do we have?

A

140ml

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3
Q

Where does the CSF go?

A

Absorbed by the arachnoid villi/granulations into the venous system

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4
Q

7 functions of CSF

A 
Buoyancy
Intracranial volume adjustment
Miconutrient and protein transfer
Buffer resevoir
Immune via cervical lymphatics
Neurotransmitter transfer
Drug delivery
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5
Q

Normal CSF characteristics

A

Clear
60% glucose of plasma
opening pressure 80-180mmH2O
Protein <= 500mg/dl

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6
Q

Name the most common reason for communicating hydrocephalus

A

Subarachnoid haemorrhage

Due to blockage of arachnoid villi with blood

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7
Q

When does idiopathic intracranial hypertension usually occur?

A

Overweight young females with headache and visual loss
Or after taking vit A, tetracyclines or withdrawal of steroids
Treatment: repeated LPs, CAi (acetazolamide), shunt surgery

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8
Q

What is the meaning of elevated rbcs found in the csf?

A

Traumatic tap or subarachnoid haemorrhage
Xanthachoromia (if bilirubin present then subarachnoid)
!!This is reliant on waiting 12 hrs after the headache began!!

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9
Q

Indications for LP

A
  • Infections of the Central nervous System: Meningitis or Encephalitis secondary to other pathogens
  • Subarachnoid Haemorrhage (SAH).
  • Inflammatory/Demyelinating CNS diseases: MS
  • Inflammatory Neuropathies: Guillain-Barré Syndrome,
  • Idiopathic Intracranial Hypertension.
  • Unexplained Pyrexia with neurological symptoms (particularly in children).
  • Infiltration of the meninges: Leukaemia, Met. Melanoma.
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10
Q

What is dangerous about LP in meningitis?

A

Brain imaging is indicated before LP in patients with who have symptoms (e.g. reduced level of
consciousness) or signs (e.g. optic disc swelling), suggestive of significantly raised ICP, or focal neurology
Due to raised ICP->coning

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11
Q

When are LPs contraindicated?

A 
Raised ICP
Soft tissue infection of lumbar spine area
Coagulopathy (high INR/low platelets)
Focal neurological signs
Hx of seizures in last week
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12
Q

How does the brain compensate for increased intracranial pressure?

A

Reducing CSF volume
Reducing blood volume (venous then arterial)
Reducing brain extracellular fluid

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13
Q

Why might intracranial pressure increase?

A 
Expanding mass (haematoma, tumour, abscess)
Increased CSF (hydrocephalus), blood (outflow obstruction) or brain (oedema)
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14
Q

How is cerebral vascular resistance altered?

A

Autoregulation (arterial contraction)

Chemoregulation (pCO2)

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15
Q

What is wrong with trying to blow off CO2 to reduce ICP?

A

Means that cerebral blood flow will reduce-> hypoxia

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16
Q

Signs of increased ICP

A

N+V (mornings, when lying flat, coughing or stooping)
Papilloedema
Reduced GCS
Cushing’s response (increase BP, decrease HR, late response)

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17
Q

Treatment of raised ICP

A 
Head up
Sedation (reduce metabolic activity of brain)
Mannitol
CSF ventricular drainage
Decompression craniectomy
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18
Q

Features of migraine

A

Typically benign and recurring syndrome with female predominance
Onset in teens
Throbbing
Unilateral (60%)
N&V, photophobia and phonophobia
Associated visual, sensory, motor or speech disturbance

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19
Q

Name some triggers of migraine

A

Alcohol, chocolate, cheese, menses, hunger, missing a meal, lack of sleep, stress, period after stress,
anxiety, worry, depression, OC pills, HRT, perfumes, glare, flashes of light, physical exertion, head trauma

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20
Q

What is the classical visual aura in migraine?

A

Scintillating scotoma (zig zags)

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21
Q

Treatment of migraine

A

Acute attack: Triptans

Prophylaxis: Beta blockers, tricyclic antidepressants, antiepileptics

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22
Q

Treatments of cluster headaches

A

Treatment: - O2 inhalation 8L/minute, Triptans, Prednisolone
Prophylaxis: - Verapamil, Lithium, Prednisolone, Sodium valproate

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23
Q

Treatment of tension headaches

A

NSAIDs and TCAs (amitriptyline)

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24
Q

What GCS is treated as coma?

A

8 or less

This is the threshold for intubation

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25
Q

Name 7 intracranial causes for coma

A

Head injury
Epilepsy
Infarction (large hemisphere stroke with secondary brainstem compression, or brainstem stroke)
Haemorrhage (intraparenchymal, pituitary, subarachnoid, subdural, extradural)
Tumour
Infection (Abscess, empyema, encephalitis, meningitis)
Hydrocephalus

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26
Q

Name 4 extracranial causes for coma

A 
Diabetic complications (hypoglycaemia, hyperosmolar non-ketotic coma)
Poisons and drugs overdose
 Organ failure (liver, kidney, lung, adrenal, thyroid, pituitary, heart)
 Ionic disturbance (hyponatraemia, hypernatraemia, hypercalcaemia)
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27
Q

Difference between a primary and secondary head injury

A

Primary brain injury: On impact, irreversible. Eg due to deceleration/rotation, shearing, contusion
Secondary brain injury: After injury, reversible. Haematoma/Raised ICP.
Intracerebral/subdural/extradural

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28
Q

Acute extradural haemorrhage features

A

Young/skull fracture rupturing middle meningeal artery or dural sinus
Lens shaped white patch on CT

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29
Q

Chronic subdural haemorrhage features

A

Elderly and alcoholics atrophic brains. Bridging veins rupture. Crescent shaped, turns dark after 2 weeks. Poor prognosis, depressed GCS
Solid goo acutely, turns liquid and can be removed with a burr hole chronically

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30
Q

2 types of primary brain injury

A

Diffuse axonal injury (DAI) (shearing forces)

Contusion (haemorrhagic)

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31
Q

What are the main viral causes of meningitis?

A

Herpes simplex, Enterovirus, Varicella

Zoster

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32
Q

What are the main bacterial causes of meningitis?

A

Streptococcus pneumoniae most common followed by N meningitidis, and H influenzae in adults
Gram negative rods and S agalactaciae are common in the very young
Listeria monocytogenes is common in neonates and elderly.

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33
Q

Symptoms of meningitis

A

fever, headache, neck stiffness, photophobia,

nausea, vomiting, and signs of cerebral dysfunction (e.g., lethargy, confusion, and coma)

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34
Q

What drugs are used for suspected meningitis?

A

IV Cefotaxime and aciclovir

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35
Q

Common organisms for CNS abscesses

A
  • pneumococcus from frontal and ethmoid sinus
  • bacteroides fragilis from chronic otitis
  • aspergillosis and murcormycosis in diabetics / immunocompromised
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36
Q

Causes of viral encephalitis

A

herpes simplex virus (HSV) – 90% of cases caused by HSV-1
Other herpes viruses – varicella-zoster (VZV), EBV, CMV, HH6
measles, mumps and rubella
arboviruses – most common worldwide is Japanese B encephalitis

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37
Q

What is delerium?

A

Acute; attentional and behavioural deficits (including hallucinosis) predominate with
impairment of memory and orientation; may show diurnal variation (often worse at night) with periods
of relative lucidity.

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38
Q

What is dementia?

A

Subacute/progressive; acquired disorder affecting two or more cognitive domains in the
absence of delirium or “non-structural” psychiatric diagnosis (e.g. depression or schizophrenia).

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39
Q

What is Wernicke-Korsakoff?

A

Encephalopathy caused by thiamine (vit B12) deficiency seen in alcoholics

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40
Q

What is seen fronto-temporal dementia?

A 
Onset 50-65yrs
Focal lobar atrophy
Personality change/disinhibition
Memory may be preserved
Can progress to aphasia
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41
Q

What is seen in Alzheimer’s Disease?

A

Tau, Beta-amyloid and plaques are seen pathologically
Degenerative dementia, increasing incidence with age
Autobiographical memory impaired, progressing to other domains

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42
Q

What is seen in vascular dementia?

A

Vascular disease risk factors (smoking/cholesterol/MI/hypertension)
Stepwise progression

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43
Q

What is seen with Lewy body dementia?

A

Alpha-synuclein protein aggregates in cortical neurons
Parkinsonism, REM sleep distrubance, depression
Memory and visuospatial deficits
Visual hallucinations (tiny green men)
Cognitive fluctuations
V sensitive to antipsychotics

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44
Q

What is a TIA?

A

Sudden onset of focal neurological deficit lasting <1hr due to a vascular origin

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45
Q

What can cause intracerebral haemorrhage?

A 
Hypertension
Amyloid angiopathy
Trauma
Bleeding disorders
Illicit drugs – amphetamines, cocaine
Vascular malformations
46
Q

What are the 3 main causes of ischaemic stroke?

A

Atherothrombotic
Small vessel disease (lipohyalinosis/fibrosis)
Cardioembolic (AF/valvular heart disease/post MI)

47
Q

What causes must you be aware of in young ischaemic stroke?

A 
Arterial dissection
Hypotension-> watershed infarct
Vasculitis
Hypercoagulability
Cocaine
Secondary to CNS syphilis/TB
48
Q

Symptoms of an L sided (dominant) MCA stroke

A

Right sided hemiparesis (leg sparing) +/- hemisensory loss
Right sided homonymous hemianopia
Dysphasia

49
Q

Symptoms of a MCA stroke when non dominant side

A

Contralateral hemiparesis+/- hemisensory loss
Contralateral homonymous hemianopia
Sensory neglect and apraxia

50
Q

Symptoms of a posterior artery stroke (vertebrobasilar)

A

Ipsilateral cerebellar signs (if cerebellar stroke)
Contralateral homonymous hemianopia (if occipital lobe)
Diplopia, hemi/quadriparesis, horner’s, sensory symptoms if brainstem stroke

51
Q

Whats a LACI?

A

Lacunar cerebral infarct
Internal capsule
Given total contralateral hemiparesis and/or hemisensory loss

52
Q

Management of acute stroke

A

O2, glucose and electrolyte monitoring, fluids
Thrombolysis (IV rTPA) within 4.5hrs if ischaemic
Swallowing assessment/NG feeds
DVT prophylaxis (hydration, stockings)
CT scan
Aspirin
Investigations for underlying cause + then treatment

53
Q

Prognosis for large MCA stroke

A

> 90% dead or dependent at 1 year

54
Q

Name 6 common causes for blackouts

A 
Vasovagal syncope
Generalised tonic-clonic seizure
Non-epileptic attack
Hyperventilation
Hypoglycaemia
Tachyarrythmias
55
Q

4 precipitants of vasovagal syncope and witness account

A

High ambient temperature, prolonged standing, large meal, pain
Prodrome of nausea, sweating, blurred vision, light headed
Collapse, pallor, usually motionless/some clonic limb movements, lasts for max 1 minute
Recovers very quickly

56
Q

Name 3 precipitants of generalised tonic-clonic seizures and witness account

A

Sleep deprivation, flashing lights, alcohol
No warning/focal aura
Tonic phase followed by synchronous jerking, cyanosis, urinary incontinence, tongue biting, attack less than 10 mins
Prolonged recovery, drowsiness/headache/confusion

57
Q

Name 2 precipitants of non epileptic attacks and witness account

A

Stressful events/induced by suggestion
Gradual onset, no aura
No cyanosis
Flailing, asynchronous and bizarre limb movements
Waxing and waning, prolonged attack
Minimal post-ictal confusion and drowsiness

58
Q

Prevalence of epilepsy

A

5.3/1000

esp early childhood and elderly

59
Q

Investigations of epilepsy

A

History
ECG
MRI (structural brain pathology?)
EEG (focal/genetic generalised)

60
Q

Name the 4 main drugs for epilepsy treatment

A

Carbamazepine (1st line for partial seizures)
Lamotrigine
Sodium valproate (doesn’t affect contraceptive pill but teratogenic)
Phenytoin

61
Q

Drugs used in status epilepticus

A

Buccal midazolam/rectal diazepam
IV lorazepam
Phenytoin
General anaesthesia if necessary (propofol)

62
Q

DVLA advice concerning epilepsy?

A

1st unprovoked seizure: if MRI normal 6 month ban
Unprovoked seizures: 1 yr ban (unless seizures only in sleep)
Stop driving for 6 months if withdrawing from AED

63
Q

Difference between Wernicke’s and Broca’s aphasia

A 
Non fluent aphasia (Broca’s): Speech output is reduced, eg 4 words. May understand but not be able to find the correct words/express. Due to damage to the left hemisphere inferior frontal gyrus
Fluent aphasia (Wernicke’s): Cannot grasp meaning of spoken word. Speech is fluent but non sensical, with irrelevant words intruding into sentences.  Due to damage to the left posterior temporal area of the brain.
64
Q

Most common causes of subarachnoid haemorrhage (SAH)

A

Trauma

Then spontaneous haemorrhage due to vascular abnormality (aneurysm)

65
Q

Most common brain tumour

A

Secondary metastasis from elsewhere (breast/lung)

66
Q

Most common primary brain tumours

A

Glioblastoma (deadly)

Meningioma (benign usually)

67
Q

Pituitary adenomas cause what?

A 
Prolactinoma: menorrhoea in women/lack of libido in men
Treated with bromocriptine analogue
ACTH secreting: Cushing's
Growth hormone: Gigantism/acromegaly
Can cause bitemporal hemianopia
68
Q

Presenting symptoms of a subarachnoid haemorrhage (SAH)

A

Sudden onset, instantly peaking, occipital ‘worst headache of my life’
Drowsiness/seizure
N+V
Meningism

69
Q

Investigations for a suspected SAH

A

CT head within 24hrs of symptoms
If unsure, LP at 12 hrs after onset of symptoms
If no trauma, CT angiogram to find aneurysm

70
Q

Treatment of SAH

A 
Resus, airway
Analgesia, antiemesis
IV hydration
Nimodipine
Neuro obs and VTE stockings
Clipping/endovascular embolisation (coiling) of aneurysm
71
Q

Name 6 factors associated with aneurysm rupture

A 
Previous rupture of same aneurysm
Rupture of contemporaneous aneurysm
Size
Posterior circulation
Smoking
Focal symptoms/evidence of growth
72
Q

Complications of SAH

A

Hydrocephalus (arachnoid granulations cannot absorb CSF)
Vasospasm
Hyponatraemia (SIADH)

73
Q

What is the basal ganglia?

A

Collection of subcortical nuclei

Caudate, putamen, globus pallidus, subthalmic nucelus, substantia nigra

74
Q

What is chorea?

A

Brief irregular rapid involuntary movement

75
Q

What is athetosis?

A

Slow, sinuous, writhing involuntary movements

76
Q

Classic triad of Parkinsonisms

A

Lead pipe RIGIDITY
Resting, pill rolling TREMOR
AKINESIA

77
Q

Name 7 causes of parkinsonism

A 
Idiopathic
Drug induced (antipsychotics)
Progressive supranuclear palsy
Wilson's disease
Huntington's disease
Carbon monoxide poisoning
Hydrocephalus
78
Q

Genetic factors in idiopathic parkinson’s?

A

Alpha-synuclein gene mutations
Parkin gene
?pesticides

79
Q

Pathology of parkinson’s

A

Degeneration of dopaminergic nigro-striatal projection with Lewy inclusion bodies
SPECT scans may help diagnosis

80
Q

Treatment of parkinson’s

A

– levodopa combined with peripheral dopa decarboxylase inhibitor (Sinemet or Madopar)
SE– nausea, drowsiness, hypotension, confusion
 dopamine agonists – used as monotherapy in early young-onset PD (pramipexole,ropinirole)
? delay onset of motor fluctuations
SE– similar to levodopa but much more prominent
Ergot alkaloids (pergolide, carbergoline) may lead to pleuro-pericardial fibrosis and valvular
heart disease
 COMT inhibitors (e.g. entacapone)
o boosts and prolongs the action of levodopa by inhibiting the metabolism of dopamine
o may be useful in patients noticing wearing off effect before next dose of levodopa is due

81
Q

What type of tremor is seen in cerebellar disease?

A

Intention tremor

82
Q

What is MS?

A

Episodic T cell inflammation of the CNS on a background of neurodegeneration
Degeneration esp affects periventricular white matter, juxtacortical white matter, optic nerves, brainstem,
cervical cord.
Can be relapsing-remitting (65%), primary progressive or relapsing progressive

83
Q

Common presenting symptoms of MS

A

Blurred vision, painful eye movements, impaired colour vision, central scotoma -> optic neuritis
Ascending numbness and parasthesia-> cervical cord
Mild bladder symptoms -> cervical cord
Vertigo, lack of coordination, diplopia-> brainstem

84
Q

Signs of MS

A 
RAPD, optic disc pallor
UMN signs (incr tone, brisk reflexes)
Cerebellar signs, internuclear opthalmoplegia
85
Q

Investigations for MS

A 
MRI T2 weighted (white dot lesions seen)
LP (oligoclonal bands uniquely in CSF)
Evoked potentials (delayed)
86
Q

Treatment of MS

A

Acute relapse: steroids (methypred), treat infection
Disease modifying:
-Interferon β + glatiramer acetate injections reduce relapse frequency
-Fingolimod, dimethyl fumarate and teriflunomide- new oral medications that reduce relapse frequency
-Natalizumab is a monoclonal antibody

87
Q

Symptomatic treatment of MS

A
  • Bladder dysfunction: oxybutynin/intermittent self-catheterization
  • Fatigue: look for depression/amantadine or modafinil
  • Depression: SSRI
  • Spasticity: baclofen or tizanidine
  • Pain and spasms: gabapentin or carbamazepine
  • Erectile dysfunction
88
Q

What is assessed in neuromuscular disease?

A 
Pain and cramps
Wasting/hypertrophy
Weakness
Myotonia
Myoglobinuria (brown urine due to rhabdomyolysis)
FH
Sensory deficits
Reflexes
89
Q

Typical myopathy presentation

A

Diseases of muscle typically result in proximal, symmetrical weakness without sensory or autonomic
symptoms

90
Q

Name some hereditary muscular dystrophies

A

Duchenne MD: X linked, dytrophin. Onset aged 5, can’t walk aged 10
Becker: milder form
Myotonic: adult, myotonia, ptosis, cataracts

91
Q

What is myasthenia gravis?

A

Caused by an antibody-mediated attack on skeletal muscle nicotinic ACh receptors-> neuromuscular transmission failure and fatiguable muscle weakness.

Fluctuating weakness involves eyes (causing ptosis and ophthalmoparesis), face, neck, oropharynx (causing dysphagia and a nasal speech), respiratory muscles and limbs (proximal > distal)
A thymoma is present in 15%

A myasthenic crisis (respiratory failure requiring ventilation) can be provoked by infection, aspiration, pregnancy, surgery, medications or emotional upset.

92
Q

Treatment of myasthenia gravis

A

Pyrodostigmine (ACh esterase inhibitor)
Steroids (immunosuppression)
Plasmapheresis

93
Q

What is MND?

A

Motor neuron disease (diffuse, chronic, partial denervation)
Classically: LMN signs of weakness, wasting and
fasciculations
May be in combination with UMN signs (amytrophic lateral sclerosis)
Median survival after diagnosis is 3 yrs, if bulbar then less

94
Q

What is radiculopathy?

A

Typically result from disk herniation and nerve root compression. Presents with radicular pain (shooting pains radiating along a dermatome, often induced by arm or leg movement) and can cause motor and sensory deficits & reflex change

95
Q

What is cauda equina syndrome?

A

Polyradiculopathy involving multiple lumbosacral nerve roots and presents with:
o Bilateral leg pain or sensory disturbances
o Perianal, perineal, and “saddle” anaesthesia
o Urinary and/or faecal incontinence
o Low back pain
o Significant bilateral motor deficit
o Sexual dysfunction

96
Q

What is carpal tunnel syndrome?

A

Compression of the median nerve at the wrist
Wrist pain that may radiate proximally to
the elbow and tingling of the first three digits. Symptoms are invariably worse at night
Treated with wrist spinlt/decompression surgery

97
Q

Describe facial palsy and causes

A

Acute unilateral facial paralysis that involves both the forehead and lower half of the face
Majority of cases are idiopathic (Bell’s palsy) or
-Herpes zoster infection of the ipsilateral geniculate ganglion (Ramsay Hunt syndrome)
-Lyme disease
-sarcoidosis
-cerebellopontine angle tumour (associated with decreased hearing or absent corneal reflex)

98
Q

What is Guillain-Barré syndrome?

A

Inflammatory demyelinating polyneuropathy
Rapidly progressive ascending paralysis, associated with cranial nerve and respiratory muscle weakness, loss of deep tendon reflexes, and distal paraesthesia/sensory loss.
Classically a demyelinating neuropathy with ascending weakness after an infection.

99
Q

What symptoms would you expect with focal seizure arising from the primary somatosensory cortex?

A

Sensory aura (eg tingling/taste/smell/sight)

100
Q

What symptoms would you expect with focal seizure arising from the temporal lobe?

A

Different thoughts/feelings/emotions/derealisation/nonsense

101
Q

Name 4 common causes of epilepsy in the UK

A

Cerebrovascular disease, brain tumour, hippocampal sclerosis, vascular malformation

102
Q

SEs of phenytoin

A

reduces effectiveness of COC pill, allergic skin rash, sedation, diplopia, hirsutism and acne, osteomalacia

103
Q

SEs of valproate

A

No interaction with COC pill. Weight gain, sedation, platelet dysfunction

104
Q

SEs of carbamazepine

A

Reduces effectiveness of COC pill. Allergic skin rash, sedation, diplopia, neutropenia

105
Q

SEs of lamotrigine

A

reduced effectiveness of COC pill. Allergic skin rash, steven-johnsons syndrome, sedation, teratogencity?

106
Q

What might mimic Guillan Barré? (5)

A
  • Acute myelopathy (eg, from compression, transverse myelitis, vascular injury)
  • Chronic inflammatory demyelinating polyneuropathy
  • Conversion disorder/hysterical paralysis
  • Human immunodeficiency virus (HIV) peripheral neuropathy
  • Neurotoxic fish or shellfish poisoning
107
Q

How is Guillain Barre syndrome diagnosed?

A

Nerve conduction studies (nerve conduction slowing, prolongation of distal latencies, prolongation/absence of F waves
LP: elevated protein >400mg/l
MRI: nerve root enhancement with gadolinium

108
Q

What features of an LP would point to a bacterial meningitis?

A

Elevated WCC, >80% polymorphonucleocytes
Low glucose
High protein
Specific pathogen microbiology

109
Q

4 risk factors for a cerebral abscess

A

Local infection in paranasal sinuses/mastoid air cells
Congenital heart disease
Haematogenous infection
Penetrating trauma

110
Q

Describe fluent aphasia

A

Fluent aphasia (Wernicke’s): Cannot grasp meaning of spoken word. Speech is fluent but non sensical, with irrelevant words intruding into sentences. Due to damage to the left posterior temporal area of the brain.

111
Q

Describe non fluent aphasia

A

(Broca’s): Speech output is reduced, eg 4 words. May understand but not be able to find the correct words/express. Due to damage to the left hemisphere inferior frontal gyrus

112
Q

Name 10 causes of a fitting patient

A

Systemic (hyponatraemia, hypoglycaemia, drug OD)

CNS (epilepsy, head trauma, haemorrhage/stroke, brain tumour, abscess, encephalitis, meningitis)

Year 4 (9 decks)

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