Neurology Flashcards
How far apart do cluster headaches occur?
4-12 weeks
What eye changes occur in cluster headache?
Miosis
Ptosis
Diagnosis of cluster headache?
MRI with contrast (clinical but sometimes brain lesions found)
Cluster headache acute management and prophylaxis
Acute
- 100% oxygen
- SC triptan
Prophylaxis
- Verapamil
Which lobes are affected by encephalitis?
Temporal
Inferior frontal
Encephalitis CSF and imaging findings
CSF
- High lymphocytes
- High protein
- PCR: HSV-1
Imaging
- MRI e.g. petechial haemorrhages
Management for encephalitis
IV acyclovir
Condition with immune-mediated demyelination of PNS, and its causes
GBS
Resp illness or diarrhoea e.g. C. jejuni
Vaccination
Does GBS have sensory symptoms?
Yes, mild (paraesthesia)
Cranial nerve and autonomic symptoms of GBS
Cranial nerve - diplopia, facial nerve palsy, oropharyngeal weakness
Autonomic - urinary retenion, diarrhoea
GBS main investigations
LP - high protein
Nerve conduction - decreased velocity
GBS management
IVIG
Plasma exchange
Supportive e.g. DVT prophylaxis, ventilation
Patient with personality change, chorea, loss of coordination. How do you diagnose?
Huntington’s disease
Clinical
40+ CAG repeats
MRI: caudate or striatal atrophy
When is hydrocephalus headache worse?
Morning
Lying down
Valsalva manoeuvre
Difference between obstructive and non-obstructive hydrocephalus and their causes
Obstructive: non-communicating
- blocked flow of CSF
- dilatation of ventricles
e.g. tumour
Non-obstructive: communicating
- increased CSF: choroid plexus tumour
- decreased reabsorption: meningitis
What type of hydrocephalus has:
Memory impairment
Urinary frequency
Balance problems
Normal pressure hydrocephalus (CSF pressure appears normal but it isn’t)
When can LP be done in hydrocephalus?
Only non-obstructive
Acute management of hydrocephalus
External ventricular drain
Long-term management of n.o. hydrocephalus
Ventriculoperitoneal shunt
Obstructive hydrocephalus management
Surgery
Palsy in intracranial hypertension
Abducens
Idiopathic intracranial hypertension management
Weight loss
Diuretics
Therapeutic LP
Motor neuron disease signs
UMN and LMN
No sensory
Sphincter muscle dysfunction late
Main 2 types of MND
Amyotrophic lateral sclerosis: corticospinal tracts
Primary lateral - loss of Betz cells, mainly UMN
MND diagnosis
Clinical
Normal motor conduction
MRI to exclude structural causes
LP to exclude inflammatory
MND management
Supportive
Drooling - amitriptyline
Resp failure - NIV
Spasticity - baclofen
Dysphagia - PEG
Pain - analgesic ladder
Riluzole - extends life by 3 months
Which conditions involves cell-mediated autoimmune demyelination of the CNS?
Multiple sclerosis
Types of MS
Relapsing-remitting
- 1-2 month acute attacks
Secondary progressive
- neurological signs between relapses
Primary progressive
- progressive deterioration from onset
MS features (motor, sensory, visual)
Motor - spastic weakness
Sensory - Lhermitte’s: paraesthesia in limbs on neck flexion
Visual - optic neuritis, Uhthoff’s (worse with increased temp), INO
MS investigations
Bloods: antibodies (anti-maltose binding protein)
CSF - oligoclonal bands, not in serum
MRI with contrast - periventricular plaques, dawson fingers
MS management (acute, and relapse risk reduction)
Acute - high-dose steroids (oral or IV)
Risk - IV natalizumab
What happen to reflexes at level and below lesion (spinal cord compression)
Absent at level
Reduced below
Investigation for spinal cord compression
MRI spine within 24 hours
Management of cauda equina
emergency decompression
Management of malignant spinal cord compression
IV corticosteroids
Radiotherapy or surgery
How to know if spinal cord injury is partial
Perianal sensation spared