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
2
Q
How much CSF do we have?
A
140ml
3
Q
Where does the CSF go?
A
Absorbed by the arachnoid villi/granulations into the venous system
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
5
Q
Normal CSF characteristics
A
Clear
60% glucose of plasma
opening pressure 80-180mmH2O
Protein <= 500mg/dl
6
Q
Name the most common reason for communicating hydrocephalus
A
Subarachnoid haemorrhage
Due to blockage of arachnoid villi with blood
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
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!!
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.
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
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
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
13
Q
Why might intracranial pressure increase?
A
Expanding mass (haematoma, tumour, abscess) Increased CSF (hydrocephalus), blood (outflow obstruction) or brain (oedema)
14
Q
How is cerebral vascular resistance altered?
A
Autoregulation (arterial contraction)
Chemoregulation (pCO2)
15
Q
What is wrong with trying to blow off CO2 to reduce ICP?
A
Means that cerebral blood flow will reduce-> hypoxia
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)
17
Q
Treatment of raised ICP
A
Head up Sedation (reduce metabolic activity of brain) Mannitol CSF ventricular drainage Decompression craniectomy
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
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
20
Q
What is the classical visual aura in migraine?
A
Scintillating scotoma (zig zags)
21
Q
Treatment of migraine
A
Acute attack: Triptans
Prophylaxis: Beta blockers, tricyclic antidepressants, antiepileptics
22
Q
Treatments of cluster headaches
A
Treatment: - O2 inhalation 8L/minute, Triptans, Prednisolone
Prophylaxis: - Verapamil, Lithium, Prednisolone, Sodium valproate
23
Q
Treatment of tension headaches
A
NSAIDs and TCAs (amitriptyline)
24
Q
What GCS is treated as coma?
A
8 or less
This is the threshold for intubation
25
Name 7 intracranial causes for coma
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
26
Name 4 extracranial causes for coma
```
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)
```
27
Difference between a primary and secondary head injury
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
28
Acute extradural haemorrhage features
Young/skull fracture rupturing middle meningeal artery or dural sinus
Lens shaped white patch on CT
29
Chronic subdural haemorrhage features
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
30
2 types of primary brain injury
Diffuse axonal injury (DAI) (shearing forces)
| Contusion (haemorrhagic)
31
What are the main viral causes of meningitis?
Herpes simplex, Enterovirus, Varicella
| Zoster
32
What are the main bacterial causes of meningitis?
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.
33
Symptoms of meningitis
fever, headache, neck stiffness, photophobia,
| nausea, vomiting, and signs of cerebral dysfunction (e.g., lethargy, confusion, and coma)
34
What drugs are used for suspected meningitis?
IV Cefotaxime and aciclovir
35
Common organisms for CNS abscesses
- pneumococcus from frontal and ethmoid sinus
- bacteroides fragilis from chronic otitis
- aspergillosis and murcormycosis in diabetics / immunocompromised
36
Causes of viral encephalitis
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
37
What is delerium?
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.
38
What is dementia?
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).
39
What is Wernicke-Korsakoff?
Encephalopathy caused by thiamine (vit B12) deficiency seen in alcoholics
40
What is seen fronto-temporal dementia?
```
Onset 50-65yrs
Focal lobar atrophy
Personality change/disinhibition
Memory may be preserved
Can progress to aphasia
```
41
What is seen in Alzheimer's Disease?
Tau, Beta-amyloid and plaques are seen pathologically
Degenerative dementia, increasing incidence with age
Autobiographical memory impaired, progressing to other domains
42
What is seen in vascular dementia?
Vascular disease risk factors (smoking/cholesterol/MI/hypertension)
Stepwise progression
43
What is seen with Lewy body dementia?
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
44
What is a TIA?
Sudden onset of focal neurological deficit lasting <1hr due to a vascular origin
45
What can cause intracerebral haemorrhage?
```
Hypertension
Amyloid angiopathy
Trauma
Bleeding disorders
Illicit drugs – amphetamines, cocaine
Vascular malformations
```
46
What are the 3 main causes of ischaemic stroke?
Atherothrombotic
Small vessel disease (lipohyalinosis/fibrosis)
Cardioembolic (AF/valvular heart disease/post MI)
47
What causes must you be aware of in young ischaemic stroke?
```
Arterial dissection
Hypotension-> watershed infarct
Vasculitis
Hypercoagulability
Cocaine
Secondary to CNS syphilis/TB
```
48
Symptoms of an L sided (dominant) MCA stroke
Right sided hemiparesis (leg sparing) +/- hemisensory loss
Right sided homonymous hemianopia
Dysphasia
49
Symptoms of a MCA stroke when non dominant side
Contralateral hemiparesis+/- hemisensory loss
Contralateral homonymous hemianopia
Sensory neglect and apraxia
50
Symptoms of a posterior artery stroke (vertebrobasilar)
Ipsilateral cerebellar signs (if cerebellar stroke)
Contralateral homonymous hemianopia (if occipital lobe)
Diplopia, hemi/quadriparesis, horner's, sensory symptoms if brainstem stroke
51
Whats a LACI?
Lacunar cerebral infarct
Internal capsule
Given total contralateral hemiparesis and/or hemisensory loss
52
Management of acute stroke
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
Prognosis for large MCA stroke
>90% dead or dependent at 1 year
54
Name 6 common causes for blackouts
```
Vasovagal syncope
Generalised tonic-clonic seizure
Non-epileptic attack
Hyperventilation
Hypoglycaemia
Tachyarrythmias
```
55
4 precipitants of vasovagal syncope and witness account
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
Name 3 precipitants of generalised tonic-clonic seizures and witness account
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
Name 2 precipitants of non epileptic attacks and witness account
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
Prevalence of epilepsy
5.3/1000
| esp early childhood and elderly
59
Investigations of epilepsy
History
ECG
MRI (structural brain pathology?)
EEG (focal/genetic generalised)
60
Name the 4 main drugs for epilepsy treatment
Carbamazepine (1st line for partial seizures)
Lamotrigine
Sodium valproate (doesn't affect contraceptive pill but teratogenic)
Phenytoin
61
Drugs used in status epilepticus
Buccal midazolam/rectal diazepam
IV lorazepam
Phenytoin
General anaesthesia if necessary (propofol)
62
DVLA advice concerning epilepsy?
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
Difference between Wernicke's and Broca's aphasia
```
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
Most common causes of subarachnoid haemorrhage (SAH)
Trauma
| Then spontaneous haemorrhage due to vascular abnormality (aneurysm)
65
Most common brain tumour
Secondary metastasis from elsewhere (breast/lung)
66
Most common primary brain tumours
Glioblastoma (deadly)
| Meningioma (benign usually)
67
Pituitary adenomas cause what?
```
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
Presenting symptoms of a subarachnoid haemorrhage (SAH)
Sudden onset, instantly peaking, occipital 'worst headache of my life'
Drowsiness/seizure
N+V
Meningism
69
Investigations for a suspected SAH
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
Treatment of SAH
```
Resus, airway
Analgesia, antiemesis
IV hydration
Nimodipine
Neuro obs and VTE stockings
Clipping/endovascular embolisation (coiling) of aneurysm
```
71
Name 6 factors associated with aneurysm rupture
```
Previous rupture of same aneurysm
Rupture of contemporaneous aneurysm
Size
Posterior circulation
Smoking
Focal symptoms/evidence of growth
```
72
Complications of SAH
Hydrocephalus (arachnoid granulations cannot absorb CSF)
Vasospasm
Hyponatraemia (SIADH)
73
What is the basal ganglia?
Collection of subcortical nuclei
| Caudate, putamen, globus pallidus, subthalmic nucelus, substantia nigra
74
What is chorea?
Brief irregular rapid involuntary movement
75
What is athetosis?
Slow, sinuous, writhing involuntary movements
76
Classic triad of Parkinsonisms
Lead pipe RIGIDITY
Resting, pill rolling TREMOR
AKINESIA
77
Name 7 causes of parkinsonism
```
Idiopathic
Drug induced (antipsychotics)
Progressive supranuclear palsy
Wilson's disease
Huntington's disease
Carbon monoxide poisoning
Hydrocephalus
```
78
Genetic factors in idiopathic parkinson's?
Alpha-synuclein gene mutations
Parkin gene
?pesticides
79
Pathology of parkinson's
Degeneration of dopaminergic nigro-striatal projection with Lewy inclusion bodies
SPECT scans may help diagnosis
80
Treatment of parkinson's
-- 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
What type of tremor is seen in cerebellar disease?
Intention tremor
82
What is MS?
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
Common presenting symptoms of MS
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
Signs of MS
```
RAPD, optic disc pallor
UMN signs (incr tone, brisk reflexes)
Cerebellar signs, internuclear opthalmoplegia
```
85
Investigations for MS
```
MRI T2 weighted (white dot lesions seen)
LP (oligoclonal bands uniquely in CSF)
Evoked potentials (delayed)
```
86
Treatment of MS
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
Symptomatic treatment of MS
- 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
What is assessed in neuromuscular disease?
```
Pain and cramps
Wasting/hypertrophy
Weakness
Myotonia
Myoglobinuria (brown urine due to rhabdomyolysis)
FH
Sensory deficits
Reflexes
```
89
Typical myopathy presentation
Diseases of muscle typically result in proximal, symmetrical weakness without sensory or autonomic
symptoms
90
Name some hereditary muscular dystrophies
Duchenne MD: X linked, dytrophin. Onset aged 5, can't walk aged 10
Becker: milder form
Myotonic: adult, myotonia, ptosis, cataracts
91
What is myasthenia gravis?
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
Treatment of myasthenia gravis
Pyrodostigmine (ACh esterase inhibitor)
Steroids (immunosuppression)
Plasmapheresis
93
What is MND?
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
What is radiculopathy?
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
What is cauda equina syndrome?
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
What is carpal tunnel syndrome?
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
Describe facial palsy and causes
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
What is Guillain-Barré syndrome?
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
What symptoms would you expect with focal seizure arising from the primary somatosensory cortex?
Sensory aura (eg tingling/taste/smell/sight)
100
What symptoms would you expect with focal seizure arising from the temporal lobe?
Different thoughts/feelings/emotions/derealisation/nonsense
101
Name 4 common causes of epilepsy in the UK
Cerebrovascular disease, brain tumour, hippocampal sclerosis, vascular malformation
102
SEs of phenytoin
reduces effectiveness of COC pill, allergic skin rash, sedation, diplopia, hirsutism and acne, osteomalacia
103
SEs of valproate
No interaction with COC pill. Weight gain, sedation, platelet dysfunction
104
SEs of carbamazepine
Reduces effectiveness of COC pill. Allergic skin rash, sedation, diplopia, neutropenia
105
SEs of lamotrigine
reduced effectiveness of COC pill. Allergic skin rash, steven-johnsons syndrome, sedation, teratogencity?
106
What might mimic Guillan Barré? (5)
* 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
How is Guillain Barre syndrome diagnosed?
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
What features of an LP would point to a bacterial meningitis?
Elevated WCC, >80% polymorphonucleocytes
Low glucose
High protein
Specific pathogen microbiology
109
4 risk factors for a cerebral abscess
Local infection in paranasal sinuses/mastoid air cells
Congenital heart disease
Haematogenous infection
Penetrating trauma
110
Describe fluent aphasia
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
Describe 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
112
Name 10 causes of a fitting patient
Systemic (hyponatraemia, hypoglycaemia, drug OD)
| CNS (epilepsy, head trauma, haemorrhage/stroke, brain tumour, abscess, encephalitis, meningitis)
