Neuro Flashcards
1
Q
What are the primary headache disorders (3)
A
Tension headache
Migraine
Cluster headache
2
Q
What are the secondary headache syndromes (8)
A
Raised ICP
Idiopathic intracranial hypertension
Hypertension
Meningeal irritation (SAH/meningitis)
Concussion
Giant cell arteritis
Sinusitis
Drugs
3
Q
CF of tension headache
A
Continuous severe pressure felt bilaterally over the vertex, occiput and eyes
Variable intensity
Non pulsatile
Occurs daily and can persist for months / years
4
Q
Management of tension headaches
A
If episodic (15d):
- paracetamol and aspirin (safety net that this can lead to a medication overuse headache)
Preventative treatment:
- low dose amitriptyline 75mg initially
Chronic:
- reassurance
- relaxation techniques
- addressing underlying stressors
5
Q
CF of cluster headache
A
Short lived episodes of severe unilateral pain typically centred on one eye
Sudden onset
Wakes patient from sleep
- red eye
- nose watering
- ptosis
- vomiting
20% will experience aura
6
Q
Aetiology for cluster headache
A
Males: females 3:1
Alcohol
7
Q
Management of cluster headache
A
Exclude secondary causes eg acute angle closure glaucoma
Subcut triptan to take at the start of an attack
Home Oxygen for use during attack
Prophylactic treatment is alcohol avoidance and verapamil
8
Q
Aetiology of migraine
A
Onset in puberty
Women to men 3:1
Associated with menstruation, OCP use, physical exercise, alcohol, cheese, chocolate, red wine, stress
9
Q
Pathogenesis of migraine
A
Vasodilation after a period of vasoconstriction correlates with onset
10
Q
Features of classical migraine with aura
A
Sense of ill health followed by a visual aura in the field of vision opposite to the side of the succeeding headache
Headache is throbbing with anorexia, nausea, vomitting and photophobia
Begins locally and spreads bilaterally
Aggravated by movement
Can last hours - days
Normal neurological exam
11
Q
Features of a migraine without aura (common migraine)
A
Classical visual / sensory aura is absent but patients may feel non specifically unwell prior to the onset of headache
12
Q
What is an ophthalmoplegic migraine
A
Migraine with 3rd / 6th nerve palsy
13
Q
What is a hemiplegic / facioplegic migraine
A
Migraine with temporary limb / facial hemiparesis
14
Q
How is a hemiplegic migraine different from a TIA
A
In TIAs the maximum deficit is present immediately and headache is unusual whereas in hemiplegic migraine there is slower progression
15
Q
Long term Migraine management
A
Full neurological exam to rule out focal neurology, raised ICP or meningism
- keep headache diary
- avoid external triggers
16
Q
Acute migraine management
A
1st line: oral NSAID / paracetamol + anti emetic
Offer oral triptan
- take as soon as symptoms
- can be intranasal if vomitting
No opioids
Follow up if triptan treatment unsuccessful
17
Q
When are triptans contraindicated
A
IHD
Uncontrolled HTN
Coronary artery spasm
18
Q
Preventative migraine management
A
Consider if migraine attacks are causing significant disability (>2 mo)
- topiramate / propranolol (1st)
- amitriptyline / anti-convulsants (2nd)
Menstrual related migraines can be treated with mefanamic acid or triptans 2d before menses
19
Q
Why should the COCP be avoided in migraines with aura
A
Increased stroke risk
Contraceptive methods that prevent menstruation can be tried to try and avoid migraine
20
Q
What is idiopathic intracranial hypertension
A
Symptoms and signs of raised ICP but no mass lesion on imaging
A disorder of CSF resorption
Causes visual disturbances (Diplopia) and headaches
Associated with pulsatile tinnitus and 6th nerve palsy
21
Q
Who does idiopathic intracranial hypertension most commonly affect
A
Young obese women
22
Q
OE of IIH
A
Bilateral papilloedema
Normal CT / MRI
LP will confirm increased CSF pressure
23
Q
Management of IIH
A
Weight loss may facilitate spontaneous remission
Trial of corticosteroids can be successful
Definitive management is a surgical shunt - prevents optic atrophy
24
Q
What is normal ICP
A
0-10mmHg
25
Causes of increased ICP
Vasogenic: increased capillary permeability
- tumour, trauma, ischaemia, infection, haemorrhage
Cytotoxic: cell death leads to oedema
Interstitial: obstructive hydrocephalus- blockage of the normal CSF outflow
26
Symptoms of raised ICP
Headache: dull persistent ache, worse on lying, present on waking, worse by coughing / straining
Vomitting
Seizures
27
Signs of raised ICP
Drowsiness / GCS deterioration
Progressive dilation of pupil on affected side
Cushings reflex is a pre terminal sign of raised ICP indicating imminent brainstem herniation
Bradycardia, hypertension, irregular breathing
28
Management of raised ICP
ABCDE
Elevate head of bed to 30-45 degrees
If intubated hyperventilate to reduce PaCO2
IV mannitol 20%
Corticosteroids if tumour
Fluid restriction
29
MOA of IV mannitol 20%
Osmotic diuretic giving a clinical effect after 20mins
Useful as a temporary measure prior to definitive management
Follow serum osmolality to adjust dosing
30
What is the best prognostic indicator in the Glasgow coma scale
Motor response
31
What are the categories and scores in the Glasgow coma scale
Motor /6
Verbal /5
Eye opening / 4
32
What is a SAH
Bleeding into the subarachnoid space that can occur at any age
33
Presentation of SAH
Thunderclap headache - over seconds, devastating intensity, often occipital
Comes on during times of transient hypertension eg physical activity or sexual intercourse
Vomitting
Photophobia
Increasing drowsiness / coma
Focal neurological signs
34
OE of SAH
Decreased GCS
Neck stiffness and meningism
35
Aetiology of SAH
Berry aneurysm (70%)
Arteriole ours malformations (10%)
No lesion found (20%)
36
What is a berry aneurysm
Developmental rather than congenital
Develops in circle of Willis and adjacent arteries
Most common in anterior communicating artery
Common in those with polycystic kidney disease
RF: smoking, FH, HTN, ehlers-Danlos, Marfans
37
What is arteriovenous malformation
A congenital collection of abnormal arteries / veins
38
SAH investigations
Bloods: FBC, U&E, LFT, ESR, clotting
CT head
Lumbar puncture: CSF will become xanthochromic - yellowish
39
Management of SAH
4 weeks bed rest
BP control
Nimodipine: CCI to prevent vasospasm, reduces mortality
IV fluids
Analgesia, anti emetics
Stool softeners to prevent straining
40
Complications of SAH
Death (30%)
Rebleed
Hydrocephalus - due to fibrosis in the CSF pathways
Cerebral vasospasm
41
Indications for lumbar puncture
Diagnosis of meningitis / encephalitis
Diagnosis of SAH
Measurement of CSF pressure
Therapeutic removal of CSF
Intrathecal drug administration
Diagnosis of miscellaneous neurological conditions
42
Contraindications to lumbar puncture
Suspicion of mass in the brain / spinal cord or raised ICP
Overlying / local infection
Congenital lesions of the lumbar spine
Problems with haemostasis
43
Lumbar puncture complications
Post LP headache - occurs in 30%, onset within 24hrs, with resolution over 2 weeks
- Is classically a constant, bilateral dull ache
Dry tap
Infection
Damage to spinal nerves
Coming of cerebellar tonsils - do not perform if ICP is raised
44
Describe the procedure of a lumbar puncture
Identify L4 space - level with tops of iliac crest
Introduce needle obliquely above L4 parallel to the place of the spine, through the interspinous ligament feeling for a give as the needle enters the subarachnoid space where CSF will begin to flow
45
Why is a lumbar puncture done at L4 level
Because spinal cord ends at L1/2 so it is rare to damage the nerves of the cauda equina
46
What is a subdural haemorrhage
A collection of blood in the subdural space following a rupture of a vein usually following a head injury although can occur spontaneously
47
What is an acute subdural haematoma
Occurs in severe acceleration-deceleration head injury often with co-existing brain damage
These patients are often young and come into hospital with a dilated pupil and no lucid interval before decreased GCS
48
Management of acute subdural haematoma
Craniotomy and early evacuation of the clot is required by neurosurgery
Patients are often seriously ill
ICU admission
ICP monitoring
High incidence of subsequent epilepsy
49
What is a subacute subdural haematoma
May occur spontaneously or after minor trauma
Can be bilateral
50
Risk factors for subacute subdural haematoma
The elderly
Alcohol abuse
Other coagulopathies
51
Clinical features of subdural haematoma
Headache
Drowsiness
Confusion
Focal neurological signs
Stupor and coma occur due to coming as ICP increases
52
Investigations for suspected subdural haematoma
CT scan
Acute subdural haematoma: classic cresenteric shape with increased density conforming to the contour of the skull. May be accompanying midline shift and compression of the ventricles
Chronic subdural haematoma: blood becomes more radiolucent and assumes a Lentiform shape similar to an extradural haematoma
53
Management of subdural haematoma
Chronic may resolve spontaneously
Definitive management may involve burr hole and placement of subdural drain or mini craniotomy and haematoma evacuation
54
What is meningitis
Inflammation of the leptomeninges usually infectious in origin
55
Aetiology of meningitis
Bacterial or viral
70% neisseria meningitidis: classic petechial rash occurs in small epidemics
Streptococcus pneumoniae - more common if skull fractures, ear disease or in those with congenital CNS lesions
Listeria monocytogenes, haemophilus influenza, staph aureus, TB
Viral: enteroviruses, HSV, VZV
56
Meningitis symptom triad
Headache
Neck stiffness
Fever
57
Symptoms that are unique to acute bacterial meningitis
High fever with rigors
Photophobia
Vomiting
Intense malaise coming on over hours
58
OE for meningitis
Kernigs sign positive: hip flexed, extend at the knee to cause pain
Brudzinski’s signs positive: passive flexion of the neck leads to flexion of the knees / hip
59
What does progressive drowsiness, literalising signs or cranial nerve lesiosn indicate in meningitis
Venous sinus thrombosis
Severe cerebral oedema
Hydrocephalus
60
Investigations for meningitis
FBC, U&E, LFT, clotting, glucose, lactate
Serum PCR for pneumococcal and meningococcal antigens
Blood cultures: do not delay abx to wait for blood cultures
LP
Throat swabs
61
What does yellowish and turbid CSF indicate on LP
Pyogenic bacterial meningitis
62
What does clear CSF indicate on LP
Viral meningitis
63
What does yellowish and viscous CSF indicate on LP
Tuberculous meningitis
64
What is meningococcal meningitis
Petechial rash usually Erythematous, non bleaching purpura
Carried in nasopharynx
Immediate IV abx should be given
65
Clinical features of viral meningitis
Almost always a benign self limiting condition which lasts 4-10 days
There may be a headache that follows for some months
66
Clinical features of TB meningitis
May present as per acute bacterial meningitis but more commonly as an insidious illness with fever, weight loss and progressive confusion / cerebral irritation eventually leading to coma
67
Risk factors for TB meningitis
Immunosuppression
Malnourishment
Multiple co-morbidities
TB contact
68
Treatment for TB meningitis
Anti tuberculoid medications for 12 months alongside corticosteroids
69
Meningitis management
LP within 1 hr
Empirical abx
If non blanching rash treat as meningococcal disease : IV benzyl penicillin
If <60 and not immunosuppressed: IV ceftriaxone
If >60 or immunosuppressed: IV ceftriaxone + IV amoxicillin
Notify public health
70
Meningitis complications (acute)
Sepsis
Hydrocephalus
Adrenal haemorrhage: Waterhouse friedrichsen syndrome
71
Meningitis complications (long term)
Brain abscess
Seizure disorders
Cranial nerve palsies: sensorineural hearing loss or gaze palsies
Ataxia / muscular hypotonia
72
What is a brain abscess
Generally very rare
Most usually a complication of otitis media / paranasal sinus infection or bacterial endocarditis
Can be a history of head trauma / neurosurgery
Presents with expanding mass lesion, fever and systemic illness
73
Treatment of brain abscess
Surgical drainage
Broad spectrum abx
High dose corticosteroids
74
Complications of brain abscess
Mortality is high
Those who do survive often develop epilepsy
75
What is encephalitis
Inflammation of the brain parenchyma
Usually viral origin
Most commonly HSV
76
CF of encephalitis
Headache
Drowsiness
Fever
Malaise
Confusion
Occasional seizures
Rarely mood changes
77
Encephalitis investigations
CT head / MRI : shows diffuse oedema in temporal lobes
LP: raised opening pressure, raised lymphocytes, raised protein, positive viral PCR
Viral serology: blood and CSF samples to confirm pathogen
78
Encephalitis management
IV Aciclovir for >10 days
79
What is epilepsy
Continuing tendency to have seizures
A seizure is a transient abnormal neurological event resulting from paroxysmal discharge of cerebral neurones
Can be partial or generalised
80
Describe the stages of a tonic clonic seizure
Aura: vague warning phase
Loss of consciousness
Tonic phase: rigidity, tongue biting, incontinence, cyanosis
Clonic phase: convulsions, frothing, jerking
Post ictal: drowsy, confusion, coma
81
What are the 3 types of generalised seizures
Tonic clonic
Absence
Tonic
82
What is an absence seizure
Typically less than 10s in 4-10yr olds
Stimulated by hyperventilation and flashing lights
Remit by puberty but pre dispose to adult epilepsy
83
What is a tonic seizure
Extended or flexed trunk
84
What is a clonic seizure
Jerking
85
Wha is a Myoclonic seizure
Brief shock like movements
86
what is an atonic seizure
Drop to the ground
87
What is a partial seizure
No impairment of consciousness
Associated with sensory aura
Temporal lobe involvement: lip smacking / chewing
Frontal lobe involvement: Motor movements, speech arrest, Jacksonian march
Parietal lobe involvement: sensory disturbances, tingling, numbness
Occipital lobe involvement: visual disturbances
88
What is a complex partial seizure
Where consciousness is impaired at some stage
89
What is temporal lobe epilepsy
Classical aura with sense of fear / deja vu and hallucinations
Confusion, anxiety and automatisms eg lip smacking, chewing
90
Secondary causes of seizures
Structural abnormalities: trauma, space occupying lesion, stroke
Developmental: cerebral palsy
Metabolic: hypo / hyper glycaemia, calcaemia, natraemia
Drugs: withdrawal, cocaine, TCAs, SSRIs, ciprofloxacin
Infection: encephalitis, HIV, syphilis
91
Immediate seizure management
Recovery position
Removing harmful objects
92
What is status epilepticus
When a seizure lasts over 3 mins or starts outside hospital and is still ongoing once in hospital
But is typically a seizure >30mins
93
Management of status epilepticus
ABCDE: 100% oxygen
IV/PR/SL lorazepam
Finger prick glucose
If alcohol suspicion: IV pabrinex
Females: preg test
Then initiate 2nd anti convulsant: IV levetiracetam / phenytoin
If >20 mins - ICU - intubate under GA
CT head, LP, cultures
94
Causes of status epilepticus
Epilepsy
Hypoxia
Stroke
Brain injury
Metabolic derangements
Infections
Eclampsia
Drug withdrawal
Toxicity
95
Investigations for seizures
Bloods: FBC, U&E, LFT, Ca, Mg, glucose
Head CT / MRI
EEG
96
Management of epilepsy
After 2 seizures start treatment
Generalised: 1st line: valproate (Lamotrigine in females child bearing)
Adjuncts may be clobazam, carbamazepine, levetiracetam
Partial seizures: 1st line carbamazepine, (Lamotrigine female)
97
What are the triggers that are important to avoid in epilepsy
Infection
Lack of sleep
Alcohol
Drugs
Hypoglycaemia
Caffeine
Stress
Flashing lights
98
MOA of valproate
Potentiate GABA and causes Na channel blockage
99
Side effects of valproate
Rash
Sedation
Weight gain
Hair loss
Tremor
Birth defects
Thrombocytopenia
Liver damage
100
Side effects of levetiracetam
Benign side effect profile
Rarely causes severe skin reactions (SJS)
101
MOA of Lamotrigine
Blocks Na channels and reduces glutamate release
102
Side effects of Lamotrigine
Not highly sedating but risk of bone marrow toxicity
Withdraw if patient develops rash or flu like symptoms
103
MOA of carbamazepine
Na channel blocker
104
Side effects of carbamazepine
Rashes
Dizziness
Double vision
Agranulocytosis
Birth defects
Liver damage
105
Side effects of phenytoin
Increased gum growth
Nystagmus
Failure of combined OC pill
106
Metabolism of phenytoin
Displays zero order kinetics thus requires therapeutic drug monitoring
Metabolism saturates at a variable level leading to disproportionate increases in plasma concentrations after this point
107
When can withdrawal of seizure medication be considered
If the patient is seizure free for 2-4yrs
Drug should be reduced in dose every 4 weeks
Patient should stop driving during withdrawal
108
What should epileptic drugs be combined with in pregnancy
5mg folic acid daily in 1st trimester
Vitamin K in 3rd trimester as there is a tendency for neonatal bleeding
109
What are the rules surrounding epilepsy and driving
Tell DVLA immediately and stop driving if had a seizure
If the attack was while awake and involved LOC - licence revoked
If after 1 seizure can reapply after 6 months
If multiple seizures can reapply after 1yr
110
What are the role of upper motor neurones
Originate in motor cortex and travel down to the brain stem or spinal cord
Fibres decussate at the level of the medulla oblongata and travel down the lateral corticospinal tract to innnervate interneurons / LMN
111
What are the role of lower motor neurons
Originate in the ventral horn of the spinal cord, receive innervation from upper motor neurones and then travel to innervate ipsilateral muscles or glands
112
Signs of LMN pathology
Weakness
Wasting
Fasciculation
Hypotonia
Hyporeflexia
113
Signs of UMN pathology
Weakness (extensor in upper limb, flexor in lower limb)
No wasting
Hypertonia, spasticity
Hypereflexia
Loss of fine motor movements
Pronator drift
Extensor plantar response
Clonus
114
LMN lesion differential diagnoses
Ventral horn pathology: MND
Peripheral nerve pathology
Muscular pathology
NMJ pathology
115
UMN lesion differential diagnoses
Vascular: stroke
Inflammatory: MS, MND
Neoplastic: tumour
Degenerative: Parkinson’s
Infective: post meningitis
Extra: drugs
116
Pathophysiology of MND
Degenerative disease of the upper and lower motor neurones in the spinal cord, cranial nerve motor nuclei and motor cortex leading to progressive loss of motor function
Mean onset 50-70
Sensory exam always normal
117
What is the amyotrophic lateral sclerosis pattern of MND
Most common
Loss of spinal and brainstem lower motor neurones and also cortical upper motor neurones
Mixed signs
There is a progressive spastic tetraparesis and added lower motor neuron signs : wasting and fasciculation
Brisk reflexes
Up going plantars
118
What is the progressive muscular atrophy pattern of MND
Neuronal loss restricted to spinal lower motor neurons, giving purely LMN signs
Painless wasting begins in the small muscles of the hands and spreads
119
What is the primary lateral sclerosis pattern of MND
Rare, disease confined to cortical UMN giving purely UMN signs
Progressive spastic tetraparesis
120
What is the bulbar presentation pattern of MND
Bulbar symptoms with preservation of limb function in early stages
Poor prognosis due to early resp involvement
121
How to diagnose MND
Clinical in the presence of progressive, mixed upper / lower motor neurone signs in multiple limbs
Bloods: rule out differentials
Spinal cord MIR: rule out myelopathy / radiculopathy
Nerve conduction studies / EMG for evidence of denervation
122
Management of MND
Educate about disease
Social and carer assessments important
Riluzole: inc pre synaptic glutamate release can increase survival in ALS patient by an average of 3-4mo
Nutritional support
Overnight NIV if resp weakness
Pneumococcal / influenza vaccines
123
Complications of MND
Fatigue
Spasticity
Pain
Mobility issues
Mental health
124
Prognosis of MND
Remission is not known
Patients diagnosed with ALS pattern MND die within 3-5yr
125
What is a muscular dystrophy
Genetically determined diseases that result in progressive deterioration
126
What are myopathies
Diverse group of conditions that are grouped due to their predominant effect on muscle
127
What is neurogenic disease
Disease of peripheral nerves or motor neurones that cause secondary skeletal muscle atrophy
128
Investigations for suspected myopathy
Serum muscle enzymes: creatine kinase - raised in muscular dystrophies and inflammatory muscle disorders
Electromyography
Muscle biopsy - can differentiate between denervation and muscular disease
129
What is duchenne muscular dystrophy
Most common muscular dystrophy
X linked recessive
30% are spontaneous mutations
Caused by mutation in the dystrophin gene making muscle fibres liable to break down with repeated contraction
130
Signs of duchenne muscular dystrophy
Onset in early childhood
- global muscle weakness
- calf psuedohypertrophy: due to fatty replacement of muscle
- gowers sign: use of hands to climb up to standing
131
Investigations for duchenne muscular dystrophy
Investigations will show raised CK
Genetic testing / muscle biopsy can confirm the diagnosis
132
Prognosis of duchenne muscular dystrophy
Poor
Patients die in late teens due to resp failure and cardiomyopathy
133
What is Becker muscular dystrophy
Less common
Produces partially functioning dystrophin
Symptoms are milder
Patients generally live until mid 40s
134
What is myotonic dystrophy
Autosomal dominant condition causes by a CI- channelopathy
Symptoms more severe with each generation due to expansion of CTG repeat
CF: muscle weakness and myotonia
Inabiltuy to relax muscles
Comes on in adolescence with facial and lower limb weakness
135
What is myotonic dystrophy associated with
Cataracts
Frontal baldness
Mental impairment
Cardiac abnormalities
136
What is polymyositosis
Inflammation of striated muscle causing proximal muscle weakness
- no pain
- wasting
- insidious or acute onset
- malaise, weight loss, fever
- difficulty squatting and climbing stairs
- can lead to resp failure
137
What is dermatomyositosis
Polymyositosis with associated skin involvement
Classic heliotrophic rash
Associated periorbital oedema
Vasculitic patches over the knuckles
138
Investigations for polymyositosis / dermatomyosis
Bloods:
- serum CK : raised
- ESR: rarely raised
- ANA: most positive
- RF: 50% are RF positive
Myositis specific antibodies
EMG
MRI
Needle muscle biopsy
139
Management of polymyositis / dermatomyositis
Prednisolone / DMARDS until clinically inactive
IVIG therapy in some cases
140
What is inclusion body myositis
Insidious onset of proximal and distal muscle wasting
Can be asymmetrical
Affects white males >50
141
Investigations for inclusion body myositis
ANA not positive
Myositis specific antigens negative
Muscle biopsy shows inflammatory infiltrate and vacuoles containing beta amyloid
142
What is myasthenia gravis
Autoimmune disorder resulting in insufficient functioning acetylcholine receptors
143
Pathophysiology of myasthenia gravis
Generation of IgG autoantibodies to the ACh receptor located on the post synaptic membrane of the motor end plates
Blocks synaptic transmission at the NMJ
Is associated with other autoimmune pathology
144
One main cause of myasthenia gravis
Thymoma
- tumour of thymus epithelial cells
145
CF of myasthenia gravis
Muscle fatigability progressively with exercise
Diplopia and ptosis
Dysphagia
Speech difficulties
Face, neck, limb girdle weakness
146
Associated factors for myasthenia gravis
Thymomas in 15%
Autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
Thymic hyperplasia
147
Investigations for suspected myasthenia gravis
Single fibre electromyography
TFT and CT for thymoma
Serum anti AChR antibody titre: raised in 90%
Tensilon test: injection of edrophonium will produce rapid improvements in features - not commonly used due to risk of cardiac arrhythmia
148
Management of myasthenia gravis
Long acting acetylcholinesterase inhibitors: pyridostigmine
Immunosuppression: prednisolone, azathioprine
Thyectomy
149
Prognosis for myasthenia gravis
May never progress past ophthalmoplegia and long periods of remission can occur
Outlook is poor if there is resp muscle involvement
150
What is radiculopathy
Pathological process affecting nerve roots emerging from the spinal cord
- produces a classic radicular syndrome with pain, sensory changes and weakness in the specific dermatomes / myotomes supplied by the particular nerve root
151
What is neuropathy
Pathological process affecting a peripheral nerve
152
What is peripheral neuropathy
Diffuse, symmetrical disease, usually beginning peripherally
Can be motor, autonomic or both
153
What is demyelinating neuropathy
Damage spares axons but affects Schwann cells
- more common in immune mediated disease such as GBS
Inferred by decreased conduction velocity
Schwann cells can regrow so will improve with treatment
154
What is axonal neuropathy
Nerve cell bodies are unable to maintain long axonal processes leading to degeneration that starts at the periphery progressing up towards nuroenal cell
Axons cannot regrow so outcomes are poor
155
Metabolic causes of peripheral neuropathy
Diabetes mellitus
B12 / folate / thiamine deficiency
Uraemia (CKD)
156
Toxic causes of peripheral neuropathy
Alcohol
Chronic liver disease
Radiation
157
Autoimmune causes of peripheral neuropathy
RA
Connective tissue disorder
Hypothyroidism
158
Inflammatory causes of peripheral neuropathy
Guillain-Barré syndrome
Chronic inflammatory demyelinating polyneuropathy
159
Drugs that can cause peripheral neuropathy
Amiodarone
Statins
Hydralazine
Phenytoin
Abx
160
Infective causes of peripheral neuropathy
Syphilis
HIV
161
Vascular causes of peripheral neuropathy
Vasculitis
162
Neoplastic causes of peripheral neuropathy
Myeloma
Paraneoplastic syndromes
163
Inherited causes of peripheral neuropathy
Charcot-Marie tooth - present before the age of 20 with progressive neuropathy
Friedrich’s ataxia - cerebellar ataxia noted in the first decade combined with UMN limb signs and peripheral neuropathy
164
What can long standing peripheral neuropathy lead to
Claw deformities of the foot (pes cavus)
Joint arthropathies (Charcot foot)
Ulceration
165
Investigations for suspected peripheral neuropathy
Bloods: FBC, U&E, LFT, HbA1c, B12, ANCA, VDRL, autoantibodies
Nerve conduction studies
LP
Peripheral nerve biopsy
166
What is guillain barre syndrome
An immune mediated demyelination of the peripheral nervous system often triggered by an infection (campylobacter)
167
Initial symptoms of guillain barre syndrome
Back / leg pain
Paralysis 1-3 weeks after an infection - infection can be trivial and unidentified
168
CF of guillain barre syndrome
Ascending weakness starts in lower limbs
Reduced / absent reflexes
Distal paraesthesia
Few sensory signs
169
Investigations for suspected GBS
Clinical
Nerve conduction studies
Raised CSF protein on LP
170
Management of GBS
Severe cases progress rapidly
Prevent pressure sores, infections, DVT
Decreased FVC may indicate ventilatory failure - intubation
SC heparin + stockings
High dose IVIG within 2 weeks
171
Prognosis of GBS
Little disability before spontaneous recovery
Complete recovery over months
Left with residual weakness
10% mortality in acute phase
Poor prognosis: old age, rapid onset of symptoms, axonal patterns of damage
172
Define stroke
An acute focal neurological deficit of cerebrovascular origin that persists >24hrs
173
Types of ischaemic stroke
Thrombotic : thrombosis from large vessels eg carotid
Embolic: blood clot but fat, air or clumps of bacteria can act as embolus - usually caused by AF
174
Types of haemorrhagic stroke
Intracerebral haemorrhage: bleeding within brain
Subarachnoid haemorrhage: bleeding on the surface of the brain
175
Risk factors for haemorrhagic stroke
Age
HTN
Arteriovenous malformation
Anticoagulants
Heavy recent alcohol intake
176
Risk factors for ischaemic stroke
Age
HTN
Smoking
Hyperlipidaemia
AF
DM
Use of oestrogen OC
177
What is a lacunar infarction
Microinfarcts caused by small vessel disease : arteriosclerosis
Usually affecting sub cortical areas eg basal ganglia
Can be asymptomatic eventually leading to vascular pseudo-Parkinsonism or vascualr dementia
178
What is global ischaemia
Infarcts at arterial boundary zones due to a global reduction in blood flow due to severe hypotension
Can cause death of the majority of neurons 24hrs after the insult with the patient remaining in vegetative state
179
What are the 3 zones of cerebral ischaemic damage
Infarct core: tissue certain to die
Oligaemic periphery: tissue that will survive due to collateral supply
Ischaemic penumbra: tissue in between can have either outcome
180
CF of stroke
Contralateral limb weakness
Facial weakness
Visual disturbances
Higher dysfunction
Rare epilepsy
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Examples of higher dysfunction
Expressive aphasia
Receptive aphasia
Apraxia
Asteregnosis
Agnosia
Inattention
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Why should serum prolactin be tested after a seizure
Elevated serum prolactin is indicative of a true seizure as oppose to a pseudo seizure
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What should be ruled out on the presence of a third nerve palsy associated with pain
Posterior communicating artery aneurysm
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What are the features of a third nerve palsy
Eye is deviated down and out
Ptosis
Pupil may be dilated
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Characteristics of Webers syndrome
Ipsilateral CN III palsy
Contralateral hemiparesis
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Which cranial nerves are affected in vestibular Schwannomas
V, VII and VIII
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Presentation of pontine haemorrhage
Reduced GCS
Paralysis
Bilateral pin point pupils
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Features of juvenile Myoclonic epilepsy
Teenage girls
Exacerbated by sleep deprivation
Daydreaming (absence seizure)
Arm jerking sharply (tonic clonic + Myoclonic)
189
Characteristics of infantile spasms
Brief spasms of sudden uncontrolled movements including flexion of the head, trunk, limbs and extension of the arms
Hypsarrhythmia on EEG
190
Differentiating feature between meningitis and encephalitis
Abnormalities in brain function are present in encephalitis but in meningitis cerebral function remains normal
191
Who should receive IV dexamethasone after meningitis
Anyone who does not have meningococcal septicaemia (a non blanching purpuric rash), septic shock, recently out of surgery or immunocompromised
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Prophylaxis for people in contact with patients with meningitis
Oral ciprofloxacin or rifampicin
