Neurology Flashcards
1
Q
Define Transient ischaemic attack
A
Rapid onset of neurological deficit, less than 24hrs.
2
Q
Define Stroke
A
Rapid onset of neurological deficit, more than 24hrs.
3
Q
Types of Stroke
A
Ischaemic.
Haemorrhagic.
4
Q
How does a Transient ischaemic attack clinically present?
A
Depends on the locations of the ischaemia.
Carotid:
Amaurosis fugax, aphasia, hemiparesis, hemisensory loss, hemianopic visual loss
Vertebrobasilar:
Diplopia, vertigo, vomiting, choking and dysarthria, ataxia, hemisensory loss, hemianopic, tetraparesis
5
Q
How does an ischaemic stroke clinically present?
A
Depends on the location of the infarct.
Cerebal hemisphere (most common): Signs contralateral to the affected side. Hemiplegia, hemisensory loss, upper motor neurone facial weakness and hemianopia
Brainstem:
complex, depending on location
Multi-infarct:
Multiple steps progressing to dementia
6
Q
How does a haemorrhagic stroke clinically present?
A
Severe headache, nausea/vomiting.
Sudden loss of consciousness
-> Stroke (see ischaemic stroke clinical presentation).
7
Q
Why is a transient ischaemic attack good?
A
It’s completely reversible
8
Q
Pathophysiology of a Transient ischaemic attack
A
Ischaemia
- > oxygen deprevation of tissue
- > transient loss of function
- > resolve
- > possible remittance
9
Q
Pathophysiology of an ischaemic stroke
A
Ischaemic
- > infarct
- > Death of neural tissue
- > Loss of functionality
10
Q
Pathophysiology of a haemorrhagic stroke
A
Primarily intracerebral haemorrhage.
Risk factors -> small vessel disease and aneurysms
-> rupture and haemorrhage.
11
Q
Cause of a Transient ischaemic attack
A
Usually passage of microemboli, which subsequently lyse, from atheromatous plaques.
Can be from the carotid, or a cardiac embolus (IE)
12
Q
Cause of an ischaemic stroke
A
Ischaemic infarction due to occlusion of a vessel, usually by an embolism of a thrombus.
13
Q
Cause of a haemorrhagic stroke
A
RF: Hypertension,
excess alcohol,
smoking
and age.
14
Q
Diagnostic test for a Transient ischaemic attack
A
Clinical. ABCD2 score (risk of a stroke).
CT: Infarction check.
15
Q
Diagnostic test for an ischaemic stroke
A
CT/MRI: rule out bleed.
16
Q
Diagnostic test for a haemorrhagic stroke
A
CT or MRI: in <24hrs.
17
Q
Treatments for a Transient ischaemic attack
A
Aspirin, clopidogrel if intolerant.
Control of hypertension.
Adjust risk factors.
Start a statin.
18
Q
Treatment for an ischaemic stroke
A
Aspirin, IV alteplase in at least 4.5 hours (thrombolytic; IV tissue plasminogen activator),
antiplatelet (aspirin -> lifelong clopidogrel),
maintain glucose,
NBM.
19
Q
Treatment for a haemorrhagic stroke
A
Stop anticoagulants.
20
Q
Define Subarachnoid haemorrhage
A
Spontaneous arterial bleeding into the subarachnoid space.
21
Q
Define Dural haemorrhage
A
Bleed into a space adjacent to the dura.
22
Q
Types of Dural haemorrhage
A
Subdural.
Extradural.
23
Q
How does a Subarachnoid haemorrhage clinically present?
A
Mostly asymptomatic until rupture
-> very immediate onset of ‘thunderclap headache’,
usually on the back of the head, with nausea, and loss of consciousness.
Possible ‘warning headaches’ days before.
24
Q
How does a subdural haemorrhage clinically present?
A
Headache,
drowsiness
and confusion (may fluctuate).
Signs of ICP.
25
How does an extradural haemorrhage clinically present?
Head injury
- > Unconscious
- > Lucid recovery
- > Rapid deterioration (with focal neurological signs),
with loss of consciousness.
26
Where does a subdural haemorrhage occur?
Beneath the dura
27
Where does an extradural haemorrhage occur?
Above the dura
28
Pathophysiology of a Subarachnoid haemorrhage
Berry aneurysms are an acquired lesion that occur most commonly at bifurcations.
Can cause a mass effect if they are large.
Rupture causes a rapid release of arterial blood into the SA space
-> increased ICP and possible CVA.
Sentinel headaches due to leaking aneurysms
29
Pathophysiology of a subdural haemorrhage
Rupture of a vein running from the hemisphere to the saggital sinus (bridging veins).
30
Pathophysiology of an extradural haemorrhage
Fractured temporal bone
- > rupture of the middle meningeal artery
- > bleed.
31
Cause of a Subarachnoid haemorrhage
Spontaneous.
70% due to rupture of berry aneurysms (usually at branch points in the circle of willis).
10% due to congenital arteriovenous malformation.
20% other vascular cause.
32
Cause of a subdural haemorrhage
Almost always head injury (often minor).
But can be delayed for up to 9 months after the incident.
33
Cause of an extradural haemorrhage
Injuries that fracture the temporal bone.
34
Epidemiology of a Subarachnoid haemorrhage
5% of strokes.
35
Epidemiology of a subdural haemorrhage
Elderly and alcoholics.
36
Diagnostic tests for a Subarachnoid haemorrhage
CT scan: Star pattern
Lumbar puncture (12hrs after symptoms):
Bloody, or Increase in pigments (xanthochromia) making it straw coloured.
37
Diagnostic test for a subdural haemorrhage
CT: Appears crescent shaped.
38
Diagnostic test for an extradural haemorrhage
CT: Appears like a convex lens.
DONT DO LP.
39
Treatments for a Subarachnoid haemorrhage
Bed rest, supportive measures for hypertension,
CCB,
IV saline to replace salts,
dexamethasone for cerebral oedema.
40
Treatments for a subdural haemorrhage
Surgical removal of the haematoma.
Mannitol: Reduced ICP in small dose.
41
Treatments for an extradural haemorrhage
Surgical drainage
Mannitol: Reduced ICP in small dose
42
Complications of a Subarachnoid haemorrhage
50% die in hospital.
43
Define epilepsy
Transient abnormal electrical activity in the brain
44
Define Parkinson's disease
Neurodegenerative loss of dopamine-secreting cells from the substantia nigra.
45
Types of epilepsy
Generalised tonic clonic (Grand mals).
Absence (Petite mals).
Myoclonic, tonic and akinetic.
Partial.
46
How does generalised tonic clonic (Grand mals) epilepsy clinically present?
Sudden onset of rigid tonic phase followed by convulsion (clonic) phase.
Back and forth rhythmically.
Tongue biting,
incontinence of urine,
followed by drowsiness/coma.
47
How does absence (Petite mals) epilepsy clinically present?
Usually childhood.
Cease activity, stares and pales.
Tends to develop into grand mals.
48
How does Myoclonic, tonic and akinetic epilepsy clinically present?
Muscle jerking (myoclonic),
intense stiffening (tonic) or cessation of movement,
falling and loss of consciousness (akinetic).
49
How does partial epilepsy clinically present?
Simple (not affecting consciousness or memory)
or complex (affecting).
Symptoms depending on focus of seizure.
50
How does Parkinson's disease clinically present?
Rest tremor, rigity and bradykinesia developing over several months.
Characteristic stoop.
Pill rolling tremor.
TRAP (tremor akinesia akinesia postural instability).
Usually one side over the other at the start.
51
Pathophysiology of epilepsy
Uncontrolled electrical activity in the brain.
Innervation of muscle fibres can cause physical movements (as per tonic clonic)
and sensory disturbance possible (particularly in partial).
52
Pathophysiology of Parkinson's disease
Progressive loss of dopamine secreting cells from the substantia nigra
-> alteration in neural circuits within basal ganglia that regulates movement.
Also loss from non striatal pathways accounts for neuropsychiatric pathology.
Thought to be due to abnormal accumulation of alpha-synuclein bound to ubiquitin which forms lewy bodies in cytoplasm.
53
Causes of epilepsy
Can be triggered by flashing lights.
Broadly unknown cause, but some genetic association.
54
Causes of Parkinson's disease
Unknown.
Some genetic link (alpha-synuclein gene and parkin gene),
some environmental link.
55
Epidemiology of Parkinson's disease
Less common in smokers.
56
Diagnostic tests for epilepsy
Short term video EEG.
CT,
MRI.
57
Diagnostic tests for Parkinson's disease
Clinical,
MRI
and CT (Atrophy of the Substantia nigra).
58
Treatment for generalised tonic clonic (Grand mals) epilepsy
AED: Sodium valproate (not in child bearing age women).
Lamotrigine.
Seizure control: Diazepam (or lorazepam).
59
Treatment for absence (Petite mals) epilepsy
AED: Sodium valproate.
Ethosuximide.
60
Treatment for partial epilepsy
AED: Lamotrigine carbamazepine, Phenytoin
Seizure control: Diazepam (or lorazepam).
61
Treatment for Parkinson's disease
L-DOPA with peripheral DOPA decarboxylase inhibitor (carbidopa).
Dopamine agonists (ropinirole)
MAO-B inhibitors: Selegiline.
62
Define Huntington's disease
AD neurodegenerative,
loss of GABA + Ach,
but dopamine spared.
63
Define a migraine
Recurrent headache for 4-72hrs with visual
and/or GI disturbance.
64
Define giant cell arteritis
Granulomatous arteritis.
65
Define Trigeminal neuralgia
Knife like pain in trigeminal sensory divisions.
66
Types of migraine
Aura
Without aura
Variant
67
How does Huntington's disease clinically present?
Rrelentlessly progressive.
Chorea.
Personality change.
Later, dementia.
Occasionally prodromal phase of psychotic and behavioural symptoms.
68
How does a migraine aura clinically present?
Characteristically unilateral.
Visual disturbance (zig zaggy lines).
Photosensitivity.
Nausea.
Sometimes premonitory symptoms.
69
How does a migraine without aura clinically present?
Characteristically unilateral.
Photosensitivity.
Nausea.
Sometimes premonitory symptoms.
70
How does a variant migraine clinically present?
Unilateral motor or sensory symptoms resembling a stroke.
71
How does giant cell arteritis clinically present?
Headache, scalp tenderness, jaw claudication.
Superficial temporal artery may be firm, tender and pulseless.
Weight loss, malaise and fever.
Blindness in 25% of untreated (amaurosis fugax).
72
How does Trigeminal neuralgia clinically present?
Severe, short lasting, paroxysmal knife/electric shock like pain in one or more sensory divisions of the trigeminal nerve.
Almost always unilateral.
Usually specific trigger (washing, shaving, eating).
73
What is giant cell arteritis associated with?
Polymyalgia rheumatica.
74
Pathophysiology of Huntington's disease
Presence of mutant Huntingtin protein
- > unknown process
- > Loss of neurones in the caudate nucleus and putamen of the basal ganglia
- > Depletion of GABA and Ach.
Dopamine spared.
75
Pathophysiology of a migraine
Changes in brainstem blood flow
- > unstable trigeminal nerve nucleus and nuclei in the basal thalamus
- > release of vasoactive neuropeptides (CGRP and substance P)
- > neurogenic inflammation; vasodilatation and plasma protein extravasation.
Aura: Cortical spreading depression is a self propogating wave of neuronal and glial depolarization that spreads across the cortex.
76
Pathophysiology of giant cell arteritis
Chronic inflammation of the medium-large arteries, particularly the aorta and its extracranial branches.
Blindness: inflammation and occlusion of the ciliary and/or central retinal artery
77
Pathophysiology of Trigeminal neuralgia
Possibly as a result of compression of the trigeminal nerve by a loop of artery or vein.
78
Cause of Huntington's disease
Autosomal dominant.
CAG repeats in Huntingtin protein gene on chromosome 4.
No. of repeats -> indicative of age of onset.
79
Cause of a migraine
Genetic and environmental factors.
Precipitants: chocolate, cheese and too much/little sleep.
80
Cause of giant cell arteritis
Unknown
81
Cause of Trigeminal neuralgia
Unknown
82
Epidemiology of Huntington's disease
Usually onset in middle age.
83
Epidemiology of a migraine
More in women.
Usually presents before 40.
84
Epidemiology of giant cell arteritis
Principally over 50s.
85
Epidemiology of Trigeminal neuralgia
Mostly in old age.
86
Diagnostic test for Huntington's disease
Genetic diagnosis
87
Diagnostic test for a migraine
Clinical.
Neuroimaging: Rule out mass lesions
88
Diagnostic test for giant cell arteritis
ESR: elevated, (50/50 rule; over 50yrs with over 50 ESR).
Histology: Temporal artery biopsy.
89
Diagnostic test for Trigeminal neuralgia
Clinical.
MRI.
90
Treatments for Huntington's disease
Treat chorea symptoms (benzodiazepines, sodium valproate)
Genetic counselling.
91
Treatments for a migraine
Passes in sleep.
Painkillers: Paracetamol / NSAIDs.
In severe: Triptans (serotonin agonists).
92
Treatment for giant cell arteritis
High dose of steroids: Oral prednisolone immediately.
93
Treatment for Trigeminal neuralgia
Anticonvulsant: Carbamazepine.
94
Complications of Huntington's disease
Death, usually from infection.
95
Define Spinal cord compression
Compression of the spinal cord.
96
Define Cauda equina syndrome
Compression of the spinal cord at the level of the cauda equina.
97
Define Multiple sclerosis
Autoimmune demyelination of the CNS.
98
Types of Cauda equina syndrome
Cord ends around L2
99
Types of Multiple sclerosis
Benign,
Relapsing-remitting,
secondary chronic progressive
and primary progressive.
100
How does Spinal cord compression clinically present?
Progressive weakness of the legs with upper motor neurone pattern and eventual paralysis.
Hours to days onset.
Arms affected if lesion is above thoracic spine.
Sensory loss below lesion.
101
How does Cauda equina syndrome clinically present?
Low back pain.
Bilateral sciatica.
Lower limb motor weakness and sensory deficit (saddle anaesthesia).
Bowel and/or bladder dysfunction.
Sexual dysfunction.
102
How does Multiple sclerosis clinically present?
Typically young adult.
Two discrete instances or more of CNS dysfunction as a result of demyelination
-> remission to normal in some weeks.
Three characteristic presentations.
Optic: blurred vision, unilateral eye pain.
Brainstem: diplopia, vertigo, dysphagia, nystagmus
Spinal cord: numbness, pins and needles. Possible spastic paresis.
Lhermitte's sign: tingling down back into limbs on the flex of the neck.
103
What is spinal cord compression?
A medical emergency
104
Is cauda equina syndrome a medical emergency?
YES
105
What happens in multiple sclerosis?
Demyelination plaques disseminated in time and space (Old McDonald Classification).
106
Pathophysiology of Spinal cord compression and Cauda equina syndrome
Pressure on the nerves prevent adequate transmission and lead to permanent damage
107
Pathophysiology of Multiple sclerosis
Inflammation, demyelination and axonal loss of oligodendrocytes.
Plaques are perivenular, and predilect to particular sites:
Optic nerve, periventricular white matter, brainstem and cerebellar connections, and cervical spinal cord.
Peripheral nerves never affected.
108
Cause of Spinal cord compression
Usually vertebral tumour (metastases from lung, breast, kidney, prostate or multiple myeloma).
109
Causes of Cauda equina syndrome
Herniation of a lumbar disc (usually L4,L5 / L5,S1).
Tumour.
Trauma.
Infection.
110
Cause of Multiple sclerosis
Precise mechanism unknown.
Inflammatory process in brain and spinal cord mediated by CD4 T cells and B cells.
Exposure to EBV in early life predisposes development.
111
Epidemiology of Cauda equina syndrome
Can occur at any age.
112
Epidemiology of Multiple sclerosis
More common in women.
More common further from the equator.
More common in the young.
Differences: Primary progressive not more common in women.
113
Diagnostic tests for Spinal cord compression
MRI.
X-ray
114
Diagnostic tests for Cauda equina syndrome
Clinical.
MRI.
PRE: sphincter tone.
115
Diagnostic test for Multiple sclerosis
MRI.
CSF: oligoclonal bands of IgG on electrophoresis
VEP: visual evoked potential.
116
Treatments for Spinal cord compression
Surgical decompression of the cord.
Correction of pathology.
Dexamethasone reduces oedema around the lesion.
117
Treatment for Cauda equina syndrome
Immediate surgical decompression,
removal of causative agent.
118
Treatment for Multiple sclerosis
Short courses of steroids (methylprednisolone),
B-interferon.
Immunosuppression (Azathioprine).
119
Define Myasthenia gravis
Autoimmune
- > Ach receptors
- > Weakness, fatiguability of ocular, bulbar and proximal limbs.
120
Define Motor neurone disease
Relentless destruction of upper motor neurones and anterior horn cells in brain and spinal cord.
121
Define Peripheral neuropathies
Neuropathy of the peripheral nerves.
122
Types of Motor neurone disease
Amyotrophic lateral sclerosis.
Primary lateral sclerosis.
Progressive muscular atrophy.
Progressive bulbar palsy.
123
Types of Peripheral neuropathiesProgressive bulbar palsy.
Autonomic
Motor
Sensory
124
How does Myasthenia gravis clinically present?
Weakness,
fatiguability of ocular (-> Ptosis),
bulbar (dysphasia, dysarthria) and proximal limbs.
Improves after rest.
125
How does Motor neurone disease clinically present?
Varies with type.
Generally: Upper limbs: reduced dexterity, stiffness, wasting of intrinsic muscles of the hand
Lower limbs: tripping, stumbling gait, foot drop
Bulbar: Slurred speech, hoarseness, dysphagia
Overall: Muscle atrophy and spasticity
126
How do Peripheral neuropathies clinically present?
Can be asymptomatic.
Diabetes: Long history of paresthesia (glove stocking), pain, weakness and wasting, autonomic symptoms; incontinence, sexual dysfunction).
Usually present as foot ulcers (constant damage due to paresthesia).
127
Which neurones does amyotrophic lateral sclerosis affect?
UMN + LMN (Most common)
128
Which neurones does primary lateral sclerosis affect?
UMN
129
Which neurones does progressive muscular atrophy affect?
LMN
130
Which neurones does progressive bulbar palsy affect?
UMN + LMN of the lower cranial nerves.
131
Pathophysiology of Myasthenia gravis
Autoantibodies to nicotinic acetylcholine receptors (anti-AChR antibodies)
or MuSK (muscle specific tyrosine kinase) at the post synaptic membrane of the neuromuscular junction, causing receptor blockade/loss.
132
Pathophysiology of Motor neurone disease
Motor neurones destroyed, namely anterior horn cells of the spinal cord and motor cranial nuclei
- > LMN and UMN dysfunction
- > Mixed picture of muscular paralysis
133
Pathophysiology of Peripheral neuropathies
Diabetes:
Hyperglycaemia damages 3 cell types; retinal endothelium, mesangial cells in glomeruli and schwann cells in perpheral nerves
(these cell types cannot regulate their glucose well, so constant hyperglycaemia causes excessive oxidation -> damage).
134
Cause of Myasthenia gravis
Often associated with thymic hyperplasia,
and in 10% a thymic tumour can be found (50% of those with thymomas have MG).
135
Cause of Motor neurone disease
Unknown.
One familial variant involves mutations in free radical scavenging enzyme copper/zinc superoxide dismutase (SOD-1).
136
Cause of Peripheral neuropathies
Acute: Guillain barre
Chronic: Diabetes, alcohol.
137
Epidemiology of Myasthenia gravis
Women more than men.
138
Epidemiology of Motor neurone disease
Middle age, more common in men.
139
Diagnostic tests for Myasthenia gravis
Anti-AChR (or anti-MuSK) antibodies in serum.
Nerve stimulation tests: characteristic decrement in evoked potential following motor nerve stimulation.
Ice test: improvement of prosis with ice pack
140
Diagnostic tests for Motor neurone disease
Clinical (fasciculation).
EMG: muscle denervation
141
Diagnostic tests for Peripheral neuropathies
Nerve conduction studies.
FBC.
Diabetes: As in DM.
142
Treatments for Myasthenia gravis
Anticholinesterases: pyridostigmine
Immunosuppressant drugs (if anticholinesterases don't work): azathioprine.
143
Treatments for Motor neurone disease
Sodium channel blocker: Riluzole, slows glutamate release
Symptomatic: Baclofen.
144
Treatments for Peripheral neuropathies
Diabetic control.
Amitriptyline for neuropathic pain.
145
Complications of Myasthenia gravis
Myasthenia crisis: weakness of the respiratory muscles.
146
Complications of Motor neurone disease
Most die in 3 years from respiratory failure due to bulbar palsy and pneumonia.
147
Nerve lesions - Define upper motor nerve lesions
Loss of function of upper motor neuron.
148
Nerve lesions - Define lower motor nerve lesions
Loss of function of lower motor neuron.
149
Nerve lesions - Define nerve root lesions
Compression of the nerve root.
150
Nerve lesions - Define cranial nerve lesions
Lesion affecting a cranial nerve.
151
Nerve lesions - Define carpal tunnel syndrome
Entrapment of the median nerve against the carpal tunnel.
152
How do upper motor nerve lesions clinically present?
Spastic weakness.
Decreased control of active movement.
Spasticity.
Clasp-knife response.
Babinski present.
Pronator drift.
153
How do lower motor nerve lesions clinically present?
Muscle paresis or paralysis.
Flaccid weakness.
Fasciculations.
Hypotonia.
Hyporeflexia.
Absent Babinski reflex.
154
How do nerve root lesions clinically present?
Tingling in the dermatome affected.
Pain, paraesthesia or weakness also possible.
155
How do cranial nerve lesions clinically present?
Depends on the nerve affected.
156
How does carpal tunnel syndrome clinically present?
Pain and paraesthesia in the hand.
Typically worse at night.
Loss of sensation on median nerve innervation.
Tinnel's sign.
Phalens test.
157
Pathophysiology of upper motor nerve lesions
Lesion of the pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves.
158
Pathophysiology of lower motor nerve lesions
Lesion of the nerve fibers travelling from the ventral horn
or anterior grey column of the spinal cord to the muscle.
159
Pathophysiology of carpal tunnel syndrome
Inflammation of the carpal tunnel
- > entrapment of the median nerve
- > pain and loss of sensation.
160
Causes of upper motor nerve lesions
Can be a result of stroke,
MS,
trauma
and cerebral palsy.
161
Cause of lower motor nerve lesions
Trauma to peripheral nerves that sever axons.
Potentially sequelae of Guillain-Barre syndrome.
162
Cause of carpal tunnel syndrome
Usually idiopathic,
can be associated with hypothyroidism, diabetes, pregnancy, obesity, rheumatoid arthritis and acromegaly.
163
Epidemiology of carpal tunnel syndrome
Most common entrapment neuropathy.
164
Diagnostic test for carpal tunnel syndrome
Clinical.
Ultrasound apparently.
165
Treatments for nerve root lesions
Nerve root injection of steroids,
surgical decompression.
166
Treatments for carpal tunnel syndrome
Surgical decompression if unlikely to improve.
Nocturnal splint and steroid injections for relief.
167
Define primary brain tumour
Tumour in the brain that arose from associated tissue.
168
Define secondary brain tumour
Tumour in the brain that metastasised there from elsewhere.
169
Types of primary brain tumour
Glioma,
meningioma,
pituitary adenoma.
170
How do brain tumours clinically present?
Progressive focal neurological deficit:
Symptoms depend on location (frontal lobe -> personality change etc).
Speed of deterioration is proportional to growth of tumour.
Raised intracranial perssure: Headaches (worse on cough/leaning forward), vomiting and papilloedema.
Epilepsy: Focal or generalised.
General cancer symptoms: Weight loss, malaise, anaemia etc.
171
Pathophysiology of brain tumours
Progressive focal neurological deficit:
Mass effect of the tumour and oedema -> impact functionality of site associated with tumour. Can destroy tissue -> rapid deterioration.
Raised ICP: As tumour grows -> downward displacement of the brain -> pressure on the brainstem (drowsiness) -> respiratory depression -> coma -> death.
False localising signs possible (see left)
Epilepsy: Tumour creates unusual electrical impulses -> seizures.
172
What are some false localising signs of brain tumours?
False localising signs:
Raised ICP or the presence of a tumour can cause healthy structures to affect adjacent ones.
E.g., Downward displacement of temporal lobe -> III or VI CN palsy.
173
Cause of primary brain tumours
Derived from the skull itself, or adjacent structures.
95% of primary tumours are Gliomas or Meningiomas (others include neurofibromas and lymphomas).
174
Cause of secondary brain tumours
Metastases from:
Bronchus,
Breast,
Kidney,
Thyroid,
Stomach,
Prostate.
175
Epidemiology of primary brain tumours
About 10% of all neoplasms.
176
Diagnostic tests for brain tumours
CT and MRI.
Positron Emission Tomography to find occult metastasis.
177
Treatments for brain tumours
Surgery: Exploration, removal or biopsy (meningiomas can be fully removed without incident)
Radiotherapy: Gliomas and radiosensitive metastases
Medical: Cerebral oedema can be reduced with corticosteroids. Epilepsy treated with anticonvulsants.
178
Define meningitis
Inflammation of the meninges.
179
Define encephalitis
Inflammation of the brain parenchyma.
180
Define herpes zoster (shingles)
Varicella zoster virus reactivation.
181
Types of meningitis
Acute bacterial
Viral
182
How does acute bacterial meningitis clinically present?
Headache, neck stiffness, fever.
Photophobia and vomiting.
Kernig's sign.
Papilloedema.
Progressive drowsiness.
If meningococcal septicaemia: Purpuric, non-blanching petechiae.
183
How does viral meningitis clinically present?
As acute bacterial meningitis clinical presentation (bar rash), but usually more benign and self-limiting.
184
How does encephalitis clinically present?
Fever,
headache,
altered behaviour
and altered mental status.
Less commonly; hemiparesis, dysphagia, seizure and coma.
185
How does herpes zoster (shingles) clinically present?
Pre-eruptive: No skin lesions, but burning itching in one dermatome.
Usually a day or two before eruption.
Eruptive phase: Skin lesions appear (infectious until dried).
Erythmatous, swollen plaques.
Rash does not cross dermatomes.
186
Why is meningitis important?
It's a notifiable disease.
187
Pathophysiology of meningitis
Infection of the meninges leads to inflammation of the tissue.
188
Pathophysiology of encephalitis
Infection of the brain parenchyma
-> inflammation.
189
Pathophysiology of herpes zoster (shingles)
After infection, the virus lies dormant in the sensory nervous system in the geniculate, trigeminal or dorsal root ganglia.
Eventually flares up -> Virus travels down the affected nerve over 3-4 days, causing perineural and intraneural inflammation.
190
Cause of acute bacterial meningitis
Infective agents can reach the meninges from ears, nasopharynx, cranial injury or by bloodstream.
Neiserria meningitis and Streptococcus pneumoniae most common cause in adults.
191
Cause of viral meningitis
Herpes simplex virus,
Enterovirus.
192
Cause of encephalitis
Often presumed viral.
Commonly herpes simplex virus,
coxsackie virus,
ECHO
and mumps.
Can be tick-borne in TBE virus.
193
Cause of herpes zoster (shingles)
Varicella-zoster.
Usually occurs in childhood, but lies dormant for years/decades.
194
Diagnostic tests for meningitis
Lumbar puncture
-> CSF culture (NOT if signs of raised ICP on CT(because of raised coning).
CT Head scan if suspicion of a mass.
195
Diagnostic tests for encephalitis
Viral serology (LP and CSF studies)
CT: Check for space-occupying lesions.
196
Diagnostic tests for herpes zoster (shingles)
Clinical,
based on rash within a dermatome.
197
Treatments for acute bacterial meningitis
Cefotaxime.
Add ampicillin if risk of listeria.
Follow up based on culture sensitivity results.
Dexamethasone to reduce long term effects.
198
Treatments for viral meningitis
Supportive therapy.
Aciclovir for herpetic infection.
199
Treatments for encephalitis
If suspected herpes simplex virus, immediately treated with aciclovir.
200
Treatments for herpes zoster (shingles)
Oral aciclovir.
