Neuro Flashcards
1
Q
What is a TIA?
A
ischaemic neurological event with symptoms lasting <24h
2
Q
Causes of TIA
A
atherothromboembolism
cardioembolism (post-mi etc)
hyperviscosity (polycythaemia, sickle-cell anaemia, myeloma)
vasculitis (rare, non-embolic cause)
3
Q
assessing risk of stroke: what does the ABCD2 score stand for?
A
A- age >60 (1pt) B- BP>140/90mmHg (1pt) C-clinical features (unilateral weakness 2pt, speech disturbance without weakness 1pt) D-duration (>60min 2pt) D- diabetes (1pt)
4
Q
Factors for high risk of stroke
A
ABCD2 score>4
atrial fibrillation
>1 TIA in a week
TIA whilst on anticoagulant
5
Q
what is amaurosis fugax
A
renal artery is occluded causing unilateral progressive vision loss (like curtain descending)
6
Q
investigations for TIA
A
bloods CXR ECG carotid doppler CT angiography
7
Q
management of TIAs
A
- control CV risk factors
- antiplatelet drug = aspirin 300mg for 2 weeks then switch to clopidogrel 75mg
- carotid endarterectomy to remove plaque build up in carotid
8
Q
Causes of stroke
A
- thrombus in situ
- cardiac emboli
- atherothroboembolism
- CNS bleeds
9
Q
risk factors for stroke
A
- high BP
- smoking
- DM, heart disease, peripheral vascular disease
10
Q
clinical manifestations of stroke
A
- worst at onset
- pointers to bleeding = meningism, severe headache, coma
- pointers to ischaemia = carotid bruit, AF, past TIA, IHD
11
Q
signs of cerebral infarcts
A
- depends on site
12
Q
signs of brainstem infarcts
A
- varied
- quadriplegia, visual/gaze disturbance, locked-in syndrome (aware but unable to respond)
13
Q
where are lacunar infarcts and what are the 5 syndromes associated?
A
- basal ganglia, internal capsule, thalamus, pons
- 5 syndromes= ataxic hemiparesis, pure motor, pure sensory, sensorimotor, dysarthria/clumsy hand
14
Q
signs of MCA occlusion
A
motor weakness, hemiplegia (paralysis of one side of body)
sensory disturbances
receptive and affective aphasia
15
Q
signs of ACA occlusion
A
frontal lobe, drowsiness, changes in logical thinking and personality
16
Q
signs of PCA occlusion
A
contralateral hemianopia
17
Q
differential diagnosis for stroke
A
head injury
hypo/hypercalcaemia
subdural haemorrhage
tumours, migraine
18
Q
investigations for stroke
A
- FAST
- CT/MRI
- ECG (AF)
- CXR (LV hypertrophy)
- Carotid doppler US (stenosis of carotid)
19
Q
treatment for ischaemic stroke
A
- thrombolysis = IV alteplase
- aspirin 2 weeks then switch to clopidogrel
- rehab and modify risk factors
20
Q
treatment for haemorrhagic stroke
A
- control BP = beta blocker (atenolol)
- surgery = clot evation
21
Q
acute management of stroke
A
- protect airway
- maintain homeostasis
- CT/MRI within 1h
- antiplatelets (aspirin 300mg) and thrombolysis (IV alteplase) once haemorrhagic stroke excluded
22
Q
primary prevention of strokes
A
control risk factors
lifelong anticoagulant in AF and prosthetic heart valves
23
Q
what does aspirin do
A
- blocks cyclooxygenase (COX)
- anti-platelet
24
Q
what does clopidogrel do
A
- anti-platelet
- makes platelets less ‘sticky’
25
causes of subarachnoid haemorrhage
- rupture of berry aneurysm
- arterio-venous malformations
- encephalitis, vasculitis, tumour invading blood vessels, idiopathic
26
what is a berry aneurysm
arise at site of bifurcations around Circle of Willis and may rupture causing subarachnoid haemorrhage
27
risk factors for subarachnoid haemorrhage
- previous aneurysm
- smoking/alcohol
- hypertension
- bleeding disorders
- polycystic kidneys, aortic coarctation, Ehlers-Danlos syndrome = associated with berry aneurysm
28
clinical presentation of subarachnoid haemorrhage
- thunder-clap headache
- precipitated by exertion
- mat be LOC or instant death
- symptoms = vomiting, collapse, seizures, come/drowsiness, photophobia
29
signs of subarachnoid haemorrhage
- neck stiffness
- Kernig's sign (stiffness of hamstrings - cant straighten leg when hip flexed)
- retinal, sub-hyaloid, vitreous bleeds
30
investigations for subarachnoid haemorrhage
- urgent CT
31
management of subarachnoid haemorrhage
- re-examine CNS often
- keep well hydrated
- nimodipine (CCB) reduces vasospasm so reduces ischaemia
- mannitol to reduce ICP
- surgery = endovascular coiling or surgical clipping
32
complications of subarachnoid haemorrhage
- re-bleeding
- cerebral ischaemia due to vasospasm
- hydrocephalus due to blockage of arachnoid granulations (needs lumbar drain)
- hyponatraemia
33
what can skull fractures cause
- may cause contusions and haematomas
| - base of skull fracture = LCN palsies or CSF discharge from nose or ear
34
what are cerebral contusions, what causes them and what can they cause
- bruises on brain surface
- from brain suddenly moving in cranial cavity and being crushed
- causes oozing of blood into brain parenchyma and can cause cerebral oedema and raised ICP
35
what is a subdural haemorrhage
- between dura and arachnoid mater
- bleeding from bridging veins between cortex and venous sinuses
- blood spreads freely in subdural space so crescent shape
- starts to break down weeks later causing increase in oncotic pressure leading to water being pulled in and growing in size
36
causes of subdural haemorrhage
minor trauma up to 9 months prior
| dural metastases, lowered ICP
37
symptoms and signs of subdural haemorrhage
- fluctuating consciousness
- physical/intellectual slowing
- sleepiness, headache, personality change, unsteadiness
- raised ICP
- seizures
38
differential diagnoses for subdural haemorrhage
- dementia
- stroke
- CNS masses
39
investigations for subdural haemorrhage
- CT/MRI
| - crescent shaped collection of blood over one hemisphere
40
management of subdural haemorrhage
- reverse clotting abnormalities
- IV mannitol to reduce ICP
- surgical removal
41
what is an extradural haemorrhage
- bleeding from middle meningeal artery after fracture of squamous temporal bone. (temple)
- accumulation of blood is slow
- characteristic lucid period
- any tear in a dural venous sinus can also cause
42
Clinical presentation of extradural haemorrhage
- appear well for several hours/days then deteriorate quickly
- low GCS from rising ICP
- increasingly severe headache, vomiting, confusion, seizure
- ipsilateral pupil dilates, coma deepens, bilateral limb weakness, breathing becomes deep and irregular
43
differential diagnosis for extradural haemorrhage
- epilepsy
- carotid dissection
- carbon monoxide poisoning
44
management for extradural haemorrhage
- urgent surgery
- IV mannitol
- care of airway
45
what is epilepsy
recurrent tendency to spontaneous episodes of abnormal electrical activity within the brain which manifests as seizures
46
what are partial seizures (simple and complex)
- localised part of one hemisphere
- simple = consciousness is not affected
- complex = consciousness is impaired
47
what are generalised seizures
- no features referable to one hemisphere
- consciousness always impaired
- absence seizures
- tonic-clonic (LOC with stiffening then jerking movements)
- myoclonic (sudden jerking)
48
what are focal seizures
- one hemisphere, often with underlying structural disease
- without LOC
- with LOC = usually from temporal lobe, postictal confusion
- evolving to a bilateral, convulsive seizure (turns into generalised seizure)
49
presentation of temporal lobe seizure
emotional disturbances, dysphagia, hallucinations, bizzare associations
50
presentation of frontal lobe seizure
motor features (peddling movements), motor arrest, dysphagia or speech arrest, post-ictal Todd's palsy (limb paralysis for hours after)
51
presentation of parietal lobe seizure
sensory = tingling, numbness, pain
| motor
52
presentation of occipital lobe seizure
visual phenomena = spots, lines, flashes
53
investigations for seizure
- look for provoking causes
- EEG
- MRI for structural lesions
- drug levels
54
what AED (anti-epileptic drug) is used for focal seizures
carbamazepine
55
what AED for generalised seizures (tonic-clonic, abscence, myoclonic, tonic)
sodium valproate
56
management of epilepsy
- monotherapy or combination therapy with AEDs
| - epilepsy surgery = vagal nerve stimulator = palliative treatment
57
what is Parkinson's disease
-neurodegenerative hypokinetic movement disorder characterised by parkinsonism, neuronal loss and Lewy bodies concentrated in substantia nigra
58
pathology of parkinsons
- normal = neurones from substantia nigra connect to the putamen and globus pallidus where they release dopamine and control movement
- lack of dopamine release and loss of dopaminergic neurones in SN
- other parts of nervous system involved
- most are sporadic but can be many genetic loci
59
clinical manifestation of parkinsonism (classical triad)
1) tremor = worse at night
2) rigidity = hypertonia
3) bradykinesia (parkinsonism) = slow to initiate movement = shuffling, pitched forward gait
- autonomic dysfunction, cognitive/behavioural disturbance, sleep disfunction (rapid eye movement sleep disorder)
60
what may patients with parkinsons develop
- dysphagia
- depression
- dementia
61
investigations for parkinsons disease
- clinical
- clinical response to dopaminergic therapy is supportive
- signs worse on one side
- MRI = atrophy of substantia nigra
62
management of parkinsons disease
- dopaminergic drugs (eg levodopa) for symptom easing but longterm use can cause seveer dyskinesias
- co-careldopa = levodopa + carbidopa
- dopamine receptor agonists = pramiprexole
- tremor management with anti-cholinergics (amantadine)
63
what is Huntington's chorea
- inherited autosomal dominant neurodegenerative disorder caused by mutation of the HTT gene
64
genetics of Huntingtons chorea
- HHT gene mutation on chromosome 4
- >36 trinucleotide repeats (CAG) = higher the number, the fuller the penetrance and earlier the onset.
- anticipation = expansion of repeats in each successive generation
65
pathology of huntingtons
- huntingtin = protein coded by HHT, expressed in all cells but highest concentration in brain and testis.
- mutated huntingtin is cytotoxic to certain cells = neurones in caudate nucleus and putamen
- atrophy and neuronal loss of striatum and cortex.
- loss of neurotransmitters
66
what neurotransmitters are lost in huntingtons
- GABA, ACh, glutamate
67
clinical manifestations of huntingtons
- chorea (uncontrolled, random , jerky movements) caused by decrease of GABA and unbalanced dopamine
- motor, neuropsychiatric and cognitive decline
68
what does huntingtons chorea always result in
dementia
69
differential diagnoses for huntingtons
SLE
| MS
70
investigations for huntingtons
- clinical
- abnormal eye movements
- chorea = random, unpredictable movements
- often parkinsonism = regidity and slowness of fine finger movements
71
management of huntingtons
- chorea and aggression= risperidone (dopamine receptor antagonist)
- depression = sertraline (selective serotonin reuptake inhibitors)
- psychosis = haloperidol (neuroeptics)
72
primary headaches
migraine, cluster, tension
73
secondary headaches
- meningitis
- subarachnoid haemorrhage
- giant cell arteritis
- idiopathic intracranial hypertension
- medication overuse headache
74
what symptoms of headache need urgent referral
- thunderclap
- seizure or new headache
- suspected encephalitis
- red eye (acute glaucoma)
- headache and new focal neurology (papilledema)
75
headache red flags
new onset and history of cancer
papilledema
cluster headache
76
headache exam
fever
altered consciousness
neck stiffness/ kernig's sign
focal neurology signs
77
clinical presentation of migraine
- unilateral, throbbing headache +/- aura
- nausea/vomiting
- sensory disturbances
78
diagnostic criteria for migraine
> 5 headches lasting 4-72h + nausea + unilateral/pulsating/ impairs routine activity
79
management of migraines
- propranolol (beta blocker) to reduce frequency (prophylactic).
- oral triptan (severe) + NSAID/paracetamol during attack
- non-pharmaceutical therapies = cold packs etc
80
what is a tension headache
- very common
| - bilateral, tightening, mild/moderate pain, not aggravated by physical activity, no nausea
81
cause of tension headache
missed meals, conflict, stress, clenched jaw, overexertion, lack of sleep, depression
82
clinical manifestations of cluster headache
- rapid onset of excruciating pain around one eye that may become watery, bloodshot, lid swelling, lacrimation, facial flushing.
- unilateral
- last 15 min - 3h (once/twice a day)
- clusters last 4-12 weeks and are followed by pain free periods of months to years
83
management of cluster headaches
- treatment = 100% oxygen for 15 min + sumatriptan sc 6mg
| - preventative = avoid triggers, corticosteroids short term, verapamil (CCB)
84
how do triptan drugs work
- used for migraines and cluster headaches
- serotonin receptor agonists
- vasoconstriction of pain sensitive intracranial vessels
85
what is the criteria for a drug overuse headache
- >15 days/month
| - use of drug for >3months (ergotamine, triptans, opioids)
86
what is the treatment for drug overuse headache
withdraw drug
87
what is giant cell arteritis
vasculitis of medium/large vessels mostly head and neck arteries in >50s
88
clinical manifestations of giant cell arteritis
- over weeks/months with fever, anorexia, weightloss
- temporal artery = headache, scalp tenderness, jaw claudication
- ocular vessels = blindness
- aortic involvement = thoracic or abdominal aortic aneurysm formation
89
investigations for giant cell arteritis
- positive temporal artery biopsies (lymphohistiocytic infiltrate and giant cells)
- ESR/CRP raised, raised platelets, low Hb
- criteria = >50y/o, new headache, temporal artery tenderness and decreased pulsation, ESR>50, abnormal biopsy
90
management of giant cell arteritis
- prednisolone PO immediately or IV methylprednisolone if evolving vision loss
main cause of death = long term steroid treatment
91
what is trigeminal neuralgia
neuralgia involving one+ of the branches of the trigeminal nerves (CNV) causing severe pain
92
triggers of trigeminal neuralgia
- washing face, shaving, eating, talking, dental prostheses
93
secondary causes of trigeminal neuralgia
- compression of trigeminal root by tumour
- hypertension
- chronic meningeal inflammation
- ms
- skull base malformation (chiari)
94
clinical manifestation of trigeminal neuralgia
- paroxysms of intense, stabbing pain, lasts seconds (1-180), unilateral, face screws up with pain
95
investigations for trigeminal neuralgia
MRI to exclude secondary causes
| clinical
96
management of trigeminal neuralgia
- carbamazepine (anticonvulsant)
| - surgery
97
causes of spinal cord compression
- secondary malignancy
| - rare = infection, cervical disk prolapse, heamatoma
98
clinical manifestations of cord compression
- bilateral leg weakness, back pain, bladder and anal sphincter involvement
- normal findings above the level of the lesion
- LMN signs at level
- UMN signs below the level
99
investigations for cord compression
MRI = definitive
biopsy of and masses
CXR for lung malignancy
bloods (FBC, ESR, B12, syphilis serology, U&E, LFT, PSA)
100
treatment for cord compression
- urgent dexamethasone in malignancy
- radio/chemotherapy
- epidural abscesses must be surgically decompressed and Abx
101
what is cauda equina syndrome
- spinal cord compression at the site of the corda equina (normally starts at L1/2)
102
causes of cauda equina syndrome
same as cord compression + congenital lumbar disc disease and lumbosacral nerve lesions
103
signs of cauda equina syndrome
- back pain, radiates down legs
- sensory loss in root distribution
- decreased anal sphincter tone and bladder/bowel incontinence
104
treatment for cauda equina syndrome
lumbar decompression surgery
105
what is multiple sclerosis
demyelinating disease of the CNS in which episodes of neurological disturbance affect different parts of the CNS at different times
106
pathology of ms
- episodes of demyelination leads to attacks of acute neurological deficit over a few days and remain for a few weeks before symptom recovery.
- in early stages the recovery is complete/almost.
- eventually, extensive axonal death results in permanent neurological disability
107
clinical presentation of ms
- variable depending on lesion site.
| - symptoms worsen with heat = Uhthoff's phenomenon
108
presentation of MS plaque in cerebral hemispheres
- large variety of symptoms and many silent lesions
109
presentation of MS plaque in the spinal cord
weakness, paraplegia, spasticity, tingling, numbness, Lhermitte's sign (electric shock sensation down back into legs), bladder and sexual dysfunction
110
presentation of MS plaques in the optic nerves
impaired vision, eye pain
111
presentation of MS in the medulla and pons
dysarthria, double vision, vertigo, nystagmus
112
presentation of MS in the cerebellar white matter
dysarthria (slur words), nystagmus, intention tremor, ataxia (slurred speach, stumbling, falling, incoordination)
113
what are the categories of MS
- relapsing/remitting course
- chronic progressive (often follows R/R)
- benign (few relapses, little disability)
114
differential diagnoses for MS
- lyme disease
| - autoimmune = SLE, primary Sjogren's syndrome
115
investigations for MS
- MRI
- CSF = oligoclonal bands of IgG on electrophoresis
- clinical
116
diagnostic criteria for MS
- 2+ CNS lesions disseminated in time and space
| - exclusion of other conditions
117
management of MS
- lifestyle = exercise, stop smoking, avoid stress
- dimethyl fumarate for mild/moderate relapsing/remitting MS
- Altemtuzumab = anti-T cell
Natalizumab = inhibits VLA-4 receptor so immune cells can't cross BBB
118
treatment for MS relapses
IV methylprednisolone
119
symptom control in MS
spasticity = baclofen
tremor = botulinum toxin type A injections for arms
bladder dysfunction = self-catheterisation
fatigue = amantadine, CBT, exercise
120
what is myasthenia gravis
- NMJ disorder
- autoimmune disease = production of auto Abs against various antigens of the NMJ
- nicotinic ACh receptor, rarely MuSK, very rarely LRPP4
121
What do 75%of people with myasthenia gravis from nAChR have
abnormality of thymus = thymoma or hyperplasia
122
pathology of myasthenia gravis
- nAChR is the receptor at the motor endplate
- auto-Abs binding to receptors limit depolarisation at the end plate and impair muscular contraction
- MuSK is involved with clustering of nAChR which is important for normal functioning
123
clinical manifestations of myasthenia gravis
- muscular fatigability
- muscle groups affected = extraocular, bulbar face, neck, limb girdle, trunk
- can be subtle
- Lambert-eaton syndrome= paraneoplastic syndrome with auto Abs against calcium channel on nerve terminal causing gait difficulties, autonomic involvement and hyporeflexia
124
investigations for myasthenia gravis
- Abs = anti-AChR Abs, MuSK Abs
- EMG = decremental muscle response to repetitive nerve stimulation.
CT to exclude thymoma
125
management of myasthenia gravis
- acetylcholinesterase inhibitors (pyridostigmine)
| - immunosuppression = treat relapses with prednisolone
126
what is myasthenic crisis and how to treat it
- life threatening weakness of respiratory muscles
- monitor forced vital capacity
- ventilatory support
- plasmapheresis or IV Ig
- identify and treat trigger (infection/ meds etc)
127
what is motor neurone disease
group of neurodegenerative diseases characterised by selective loss of motor neurones.
128
what are the 4 clinical patterns of MND
1) ALS/ amyotrophic lateral sclerosis
2) progressive bulbar palsy
3) progressive muscular atrophy
4) primary lateral sclerosis
129
MND: what is amyotrophic lateral sclerosis
- loss of motor neurones in the motor cortex and anterior horn of the cord
- combined UMN + LMN signs
130
MND: what is progressive bulbar palsy
- affects cranial nerves IX - XII
131
MND: what is progressive muscular atrophy
- anterior horn cell lesion
- LMN signs only
- distal muscle groups first
132
MND: what is primary lateral sclerosis
- rare
- loss of Betz cells in motor cortex
- mainly UMN signs - spastic leg weakness and pseudobulbar palsy
- no cognitive decline
133
pathology of MND
little known
| - defects in RNA metabolism due to lack of RNA binding proteins (TDP-43 and FUS)
134
clinical manifestations of MND
- asymmetric weakness, wasting, fasciculations and spasticity of limb muscles
- difficulty swallowing, chewing, speaking, coughing and breathing
- cognitive changes
135
clinical features of LMN lesions
- muscle tone reduced = flaccid
- muscle wasting
- fasciculations (visible spontaneous contraction of motor units)
- hyporeflexia
- everything goes DOWN!
136
clinical features of UMN
- muscle tone increased (spasticity)
- hyperreflexia (jaw jerk)
- Babinski sign = extensor plantar response (toes fan out)
- upper limb extensors weaker
- lower limb flexors weaker
- emotional liability
- everything goes UP!
137
investigations for MND
- no diagnostic test
- brain/cord MRI to exclude structural causes
- neurophysiology can detect subclinical denervation
138
management of MND
- progressive and fatal within years
- multidisciplinary
- riluzole = inhibits glutamate release
- augmentive and alternative communication equipment
- palliative care
139
what is guillian-barre syndrome
classical GBS is an acute demyelinating polyneuropathy which usually follows 1-2 weeks after an upper resp tract or GI infection
140
common triggers of GBS
- clostridium jejuni, mycoplasma, CMV, HIV, VZV, EBV
| - vaccination, surgery, malignancy
141
pathology of GBS
- immune response mounted to an antigen on a pathogen cross-reacts with components of the peripheral nerve (myelin)
- demyelination
142
clinical manifestations of GBS
- few weeks after an infection a symmetrical ascending muscle weakness starts
- sudden onset of tingling and numbness of fingers and toes
143
investigations for GBS
lumbar puncture shows raised CSF protein with normal cell count
144
management of GBS
IV Ig
145
acute and chronic peripheral neuropathies
- acute = evolve rapidly and patients seek A&E
| - chronic = small fibre or large fibre (axonal or demyelinating)
146
common peripheral mononeuropathies
- carpal tunnel syndrome (median nerve)
- ulnar neuropathy (entrapment at cubital tunnel)
- peroneal neuropathy (entrapment at the fibular head)
- cranial (III or VII cranial nerve palsy)
147
what is ataxia
poor balance
sensory (loss of proprioception) or cerebellar
if sensory, ataxia worsens when eyes closed
148
motor symptoms of peripheral neuropathies
- muscle cramps
- weakness
- fasciculations
- atrophy
- high arched feet
149
symmetrical peripheral neuropathy presentation
- longer fibres affected first
- initially sensory then sensorimotor
- most common
150
asymmetrical sensory peripheral neuropathy presentation
- patchy distribution of symptoms
| - dorsal root ganglia are affected
151
asymmetrical sensorimotor peripheral neuropathy presentation
- very uncommon
- multiple nerve involvement
- mononeuritis complex
152
difference between demyelinating and axonal neuropathies
- demyelinating = slow conduction velocities
| - axonal = reduced amplitudes of the potentials
153
causes of axonal PN
- associated with systemic disease (diabetes, B12 deficiency, coeliac, chronic renal disease, alcohol, hypothyroid, amyloidosis, paraneoplastic, connective tissue disease, paraproteinemia)
- inflammatory
- infectious (hepatitis, HIV, Lyme)
- ischaemic (vasculitis)
- metabolic
- hereditary (CMT, HLPP)
- toxins (B6, environmental toxins)
154
chronic demyelinating PN
- immune mediated = CIDP (chronic inflammatory demyelinating polyneuropathy), multifocal motor neuropathy
- genetic = Charcot Marie Tooth disease (foot drop, hammer toe, leg muscle wasting)
155
acute polyneuropathies
- Guillain Barre syndrome (rapidly ascending paralysis and sensory deficits after disease)
156
treatment for PN
- symptomatic = quinine (cramps), pain, physio
| - identify reversible cause
157
signs of median nerve C6-T1 lesion/neuropathy
unable to grip
158
signs of ulnar nerve C7-T1 lesion/neuropathy
- vulnerable to elbow trauma
| - sensory loss of medial 1.5 fingers
159
signs of radial nerve C5-T1 lesion/neuropathy
wrist and finger drop
| unable to open fist
160
signs of brachial plexus lesion/neuropathy
pain/paraesthesia and weakness in affected arm
161
signs of phrenic nerve C3-C5 lesion/neuropathy
orthopnoea (SOB while laying flat) with raised diaphragm on CXR
162
signs of lateral cutaneous nerve of the thigh L2-3 lesion/neuropathy
paraesthesia
163
signs of sciatic nerve L4-5 lesion/neuropathy
- foot drop
| - loss of sensation below the knee
164
signs of common perineal nerve L4-S1 lesion/neuropathy
- foot drop
- weak ankle
- sensory loss of foot
165
signs of tibial nerve L4-S3 lesion/neuropathy
inability to stand of tiptoe, invert foot or flex toes
166
upper motor nerve lesions
- damage to motor pathways (corticospinal tract)
- affects muscle groups
- nerve cells in precentral gyrus of frontal cortex - internal capsule - brainstem and cord - synapse with the anterior horn cells in the cord
167
signs of upper motor nerve lesions
- no muscle wasting
- loss of fine finger movement
- spasticity in arm flexors and leg extensors
- hyperreflexia
- upgoing plantars
- +/- clonus (rhythmic beat of foot on dorsiflexion)
- +/- Hoffman's reflex (flexion on thumb and index finger in pincer movement following a flick to the middle finger)
168
lower motor nerve lesions
- damage anywhere from anterior horn cells in cord, nerve roots, plexi or peripheral nerves
-
169
signs of LMN lesions
- wasting and fasciculations in affected muscles
- hypotonia/flaccidity
- hyporeflexia
- plantars remain flexed
170
causes of cranial nerve lesions
- diabetes mellitus
- stroke
- MS
- tumours
- sarcoidosis
- vasculitis
- syphilis
171
CN I lesion
- olfactory
- anosmia
- from resp tract infection, trauma, meningitis, frontal lobe tumour
172
CN II lesion
- optic
- monocular blindness
- bilateral blindness
- bitemporal hemianopia
- homonymous hemianopia (affects visual field contralateral to lesion)
- optic neuritis
- ischaemia papillopathy (from stenosis of posterior ciliary artery)
- papilloedema
- optic atrophy (pale optic disc)
173
CN III lesion
- oculomotor
| - ptosis, large pupil, eye down and out
174
CN IV lesion
- trochlear
| - horizontal diplopia
175
CN V lesion
- trigeminal
- jaw deviated to side of lesion
- sensory loss
176
CN VI lesion
- abducens
| - nystagmus
177
CN VII lesion
- FACIAL
- lower 2/3 of face will droop if UMN lesion
- one side of face drops if LMN
- loss of taste
178
CN VIII lesions
- vestibulocochlear
| - problems with hearing, balance and vertigo
179
CN IX and X lesions
- glossopharyngeal and vagus
- gag reflex problems
- brainstem lesions
180
CN XI lesions
- acccessory
- unable to shrug shoulders against resistance or turn head
- innervates trapezius and sternocleidomastoid
181
CN XII lesion
- hypoglossal
| - tongue deviates to side of lesion
182
3 presenting signs of brain tumour
- raised ICP (headache, reduced consciousness, nausea and vomiting)
- progressive neurological deficit
- epilepsy
183
features of the raised ICP headache
- worst on waking in the morning
- increased by coughing, straining and bending forwards
- sometimes relieved by vomiting
184
cardinal physical signs of brain tumour
- papilledema due to obstruction of venous return from the retina
- loss of crisp optic nerve head
- venous engorgement
- retinal oedema
- haemorrhages
185
secondary brain tumours
- more common
| - most from lung
186
primary brain tumours
- most glial cell origin = astrocytoma, oligodendroglioma
187
grading of gliomas
- I = pilocytic astrocytoma (paediatric)
- II = benign premalignant tumour
- III = anaplastic astrocytoma
- IV = glioblastoma multiforme (gbm)
- all gliomas would eventually become GBM
188
treatment of glioblastomas
- resective surgery if possible
- adjuvant chemo (temozolomide) with RT then followed by more chemo
- dexamethasone improves brain function and decreases inflammation
- gene therapy (inoculation of tumour with replication deficient HSV-1 retrovirus)
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what is an astrocytoma
- CNS tumour formed by glial cells showing astrocytic differentiation
- most frequent primary brain tumour in adults
- diffuse astrocytoma's WHO grade II
- anaplastic astrocytoma WHO grade III
- glioblastoma WHO grade IV
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what is an oligodendroglioma
- diffusely infiltrative CNS tumour formed by glial cells showing oligodendroglial differentiation
- can be classical (II) or anaplastic (III)
- calcification on scan
- from neural stem or progenitor cells
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what is an ependymoma
- CNS tumour composed of neoplastic ependymal cells from the ependymal-linked ventricular system or the spinal cord.
- classical or anaplastic (III)
- genetic mutations on chromosome 22
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what is a meningioma
- tumour from meningothelial cells which is attached to the inner surface of the dura matter
- majority are benign (I) and sporadic
- slow growing
- anaplastic meningiomas are aggressive malignant tumours
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what is a medulloblastoma
primitive embryonal tumour of the cerebellum (IV)
highly malignant
children
194
what are primary CNS lymphomas
- primary extra nodal lymphomas arising in the CNS
| - immunocompromised at increased risk (EBV plays role)
195
what is meningitis
infection of subarachnoid space and inflammation of the meninges
196
what viruses can cause meningitis
echoviruses, EBV, herpes simplex, mumps
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what bacteria can cause meningitis
- neisseria meningitidis or streptococcus pneumonia
| - neonates = e.coli and group B streptococci
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pathophysiology of meningitis
1) blood - CSF - brain barrier
2) bacteria in CSF isolated from immune cells
3) replication
4) blood vessels become leaky
5) inflammation
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clinical manifestations of meningitis
```
headache
fever
neck stiffness
photophobia
more sever in bacterial infection
non-blanching purpuric rash
```
200
investigations for meningitis
- examination of CSF from lumbar puncture (DO NOT do if symptoms of raised ICP)
- predominance of lymphocytes in viral
- many neutrophils in bacterial
201
management of viral meningitis
usually runs a mild course with complete recovery
202
management of bacterial meningitis
life threatening
antibiotics (cefotaxime or ceftriaxone)
IV dexamethasone
203
immediate hospital management of meningitis
1. assess GCS
2. blood cultures
3. broad spec Abx (cefotaxime)
4. steroids : IV dexamethasone
5. lumbar puncture (microscopy, gram stain, culture, protein, glucose, viral PCR)
204
what is encephalitis
infection of the brain parenchyma and inflammation of the brain
205
causes of encephalitis
- HSV most common cause
- autoimmune, paraneoplastic
- bacterial meningitis
- TB
- Malaria
- lyme disease
206
pathology of HSV encephalitis
- following reactivation of the virus in the trigeminal ganglion where it passes into the temporal lobe
207
clinical manifestation of encephalitis
- precedes flu symptoms
- confusion
- behavioral changes
- low GCS or coma
- seizures
208
investigations for encephalitis
- bloods
- MRI of brain
- lumbar puncture = viral PCR on lymphocytic CSF sample
- urgent EEG
209
management of encephalitis
- urgent antivirals (acyclovir)
| - symptomatic and supportive treatment
210
pathology of herpes zoster (shingles)
- varicella-zoster virus (VZV) highly infectious and causes chickenpox in children
- transmitted by respiratory droplets
- infection is lifelong due to viral latency within sensory ganglia
- reactivation of virus in adults leads to shingles
211
clinical manifestations of chicken pox
```
fever
malaise
headache
abdominal pain
pruritic rash = erythematous macules for vesicles and crust
```
212
clinical manifestation of shingles
- band like vesicular eruption along the distribution of a sensory nerve (macular = dermatomal distribution)
- painful, hyperaesthetic area
- infectious until scabs appear
213
investigations for shingles
- clinical
| - in immunocompromised use viral PCR, culture, immunofluorescence
214
treatment of shingles
- acyclovir/valaciclovir (IV in immunosuppressed)
| - vaccination in elderly to prevent reactivation
215
what is dementia
- neurodegenerative
- progressive decline in several cognitive domains
- alzheimer's, lewy body, vascular, fronto-temporal
216
what is frontotemporal dementia
- frontal and temporal atrophy
- loss of >70% of spindle neurons
- behavioural/personality change, disinhibition, hyperorality, emotional unconcern
217
investigations for dementia
- look for reversible causes (raised TSH, low B12/folate)
- check MSU, FBC, ESR, U&E, LFT and glucose
- MRI
- functional imaging
218
pathology of vascular dementia
- small vessel disease may cause chronic ischaemia and diffuse white matter injury
- multiple infarcts from vascular occlusion
219
presentation of vascular dementia
- impairment of executive function and slowing of mental processing
- stepwise progression and focal neurology
220
pathology of Lewy body dementia
- accumulations of Lewy bodies within neurones of cortical grey matter and subcortical nuclei leads to damage and cell loss
221
presentation of Lewy body dementia
- progressively worsening dementia similar to Alzheimer's
- fluctuating levels of cognition, recurrent visual hallucinations, parkinsonism, hypersensitivity to neuroleptics
- autonomic nervous system problems and sleep disorders
222
what is Alzheimer's
- dementia
| - neuronal loss in the cerebral cortex associated with amyloid plaques and neuro-fibrillary tangles
223
aetiology of Alzheimer's
- accumulation of beta-amyloid peptide and tau protein results in neurofibrillary tangles, amyloid plaques and loss of ACh
- mostly in hippocampus, amygdala, temporal neocortex, and subcortical nuclei.
224
temporal lobe
- hearing (superior temporal lobe)
- language comprehension (superior temporal lobe)
- semantic knowledge (anterior temporal lobe)
- memory (hippocampus)
- emotional/effective behaviour (limbic system)
225
clinical presentation of Alzheimer's
- memory loss
- increasing disability to perform daily tasks
- agnosia (can't recognise self in mirror)
- psychotic symptoms
- loss of motor skills
- agitation, restlessness, wandering, disinhibition
- terminal stages= reduced speech, immobility, incontinence
226
management of Alzheimer's (medications)
- acetyl choline esterase inhibitors (rivastigmine)
- memantine (anti-glutamate)
- antipsychotics if very severe
