Medicine - Neurology Flashcards
Define ‘seizure’ and ‘epilepsy’
seizure = transient occurrence of S/Sx due to abnormal neuronal activity in the brain Epilepsy = at least 2 unprovoked episodes of a seizure caused by spontaneous, intermittent, abnormal electrical activity in the brain
What is the pathophysiology of epilepsy?
Imbalance between excitatory (glutamate/aspartate) and inhibitor (GABA) signalling
Commonest at the extremes of life, and 2/3rds are idiopathic
What are the two main types of epilepsy?
Focal and generalised
Describe focal epileptic seizures and the subtypes
area of local cortical abnormality in an otherwise normal brain
originates in 1 hemisphere
EEG shows localised discharge and they are easy to diagnose as features correlate to one area e.g. visual/jerking…
3 subtypes:
- without impaired consciousness
- with impaired consciousness
- evolving to bilateral convulsive seizures
Describe generalised epileptic seizures and the subtypes
Originate in one brain area but rapidly spread to involve bilateral networks, show widespread electrical discharge throughout with no features attributable to a single hemisphere. Usually as patients are born with an issue in neurotransmitter metabolism/ion channels which leads to CNS hyper-responsiveness
4 subtypes:
- absence seizures (<10s, always start in childhood, often mistaken for poor concentration at school)
- myoclonic seizures (sudden involuntary muscle group contractions, may cause patients to fall over, usually provoked e.g. alcohol, tired)
- tonic clonic seizures (pt becomes rigid (tonic) and then begins jerking (clonic), may have tongue biting, unconsciousness, headache afterwards)
- atonic (akinetic) seizures (brief loss in muscle tone, usually resulting in heavy falls +/- LOC)
What are possible triggers for seizures?
missed drugs sleep deprivation alcohol exhaustion infection flickering lights
What are the differentials for seizure/epilepsy with LOC?
migraine
panic attack
syncope
NEAD (non-epileptic attack disorders)
What are the key questions to think about when investigating epilepsy?
1) where is the epilepsy arising from? = EEG
2) what is the cause of the epilepsy? = structural (CT/MRI), metabolic (bloods), infection/inflammation (bloods, CXR, CSF)
3) are the attacks truly epileptic? = ambulatory EEG, videotelemetry
What are the three types of epilepsy treatment?
1) Lifestyle
- psychosocial therapies
- avoid triggers
2) Pharmacological
- carbamazepine
lamotrigine
levetiracetam
pregablin
gabapentin
phenytoin
sodium valproate
benzos
3) Surgery
- considered if a single epiletogenic focus can be identified e.g. low grade tumour
Which AED are Na channel antagonists?
Carbamazipine
Lamotrigene
Phenytoin
Which AED are Ca channel antagonists?
Pregablin/gabapentin
Which AED are SVA2 vesicle antagonists which stops neurotransmitter release?
Levetiracetam
Which AED are GABA metabolism inhibitors?
Sodium valproate
How do benzodiazepines work?
GABA agonists, reduce post-synaptic excitability, used in epilepsy
What is status epilepticus and how is it treated?
life threatening, continuous seizures without regaining consciousness after 5+ minutes
Cruicial to recognise as rapid termination helps prevent serious brain injury
Treatment:
A-E
Bloods (FBC, coag, BM, U&E, LFT, anti-epileptic drug levels)
If seizure >5 mins: diazepam/lorazepam
If seizure >30 mins: phenytoin loading, thiamine, glucose, benzodiazepines, general anaesthetic
One the status is controlled, commence long term anti-convulsant therapy
Define a stroke, its two types:
Sudden death of brain cells (caused by hypoxia from ischaemia/haemorrhage) leading to focal neurological deficit in a defined vascular distribution
90% ischaemic = small vessel occlusion due to thrombus/embolus
10% haemorrhagic
What are the risk factors for a stroke?
HTN!!!!!! smoking PVD DM OCP hyperlipidaemia increased clotting tendancies
Describe the 4 classifications of stroke and their features:
1) TACS = total anterior circulation syndrome (ICA/prox MCA occlusion) which presents with:
- hemianopia
- hemiparesis
- higher cortical dysfunction
2) PACS = partial anterior circulation syndrome (MCA occlusion) which present with:
- 2H’s
- higher cortical dysfunction
3) POCS = posterior circulation syndrome (PCA/cerebellar communicating artery) presents with:
- isolated hemianopia
- brainstem syndrome
4) LACS = lacunar syndrome (perforating artery/small vessel damage) present as:
- pure motor/sensory stroke
What are the differentials for a stroke?
head injury hypo/perglycaemia subdural haemorrhage tumour migraine drugs encephalopathy
What is the immediate management strategy of a stroke?
Airway (if GCS < 8 = airway management) Breathing - CXR, ABG CIrculation (HR, BP, ECG?AF) IV access and bloods (FBC, U&E, coag screen, lipids) Disability (glucose) Everything else (full neuro exams)
CT head -> rule out haemorrhage! Then if ischaemic…
- if <4.5hrs since onset: tPa (alteplase), use NIHSS score, then CT 24hrs later to check there has not been any haemorrhage
- if >4.5hrs since onset, give dual antiplatelet therapoy (aspirin/clopidogrel)
Thrombectomy may be used for pts who have/have not received thrombolysis (with alteplase)
What are 5 contra-indications to thrombolysis?
pt on warfarin/doacs intracranial haemorrhage coagulopathy recent head trauma patient has severe HTN (>200mmHg systolic) history of ischamic heart disease
What is involved in the later management of a stroke?
- swallow screen within 24hrs
- try to work out the cause: 24hr ECG tape (?paroxysmal AF), carotid doppler (?stenosis), DM?, ECHO (?patent foramen ovale)
2o prevention:
- Antiplatelet/anticoagulation
- BP lowering medications
- Cholesterol lowering (statins - atorvastatin 80mg), smoking cessation, carotid revascularisation
- diet
- exercise
What is the definition of a TIA?
transient ischaemia attack
usually due to an ischaemic (embolic) event where symptoms last <24hrs (in a stroke symptoms last >24hrs)
*Prompt management is KEY as without intervention a proportion of patients will go on to develop a stroke within 1/52
What are the 4 causes of a TIA?
Atheroembolism (e.g. from carotid artery)
Cardioembolism (post MI, AF, prosthetic valve)
Hyperviscosity (myeloma, sickle cell disease)
Vasculitis (rare, non-embolic cause of TIA symptoms)
How is a TIA managed and what risk scores are used?
(same investigations as a stroke)
Usually managed in the same way as a stroke, but patient will be asymptomatic/their symptoms will have passed by the time they are in hospital
1) control RFx: BP, lipids, smoking cessation, diet
2) antiplatelet medications: aspirin, clopidogrel
3) carotid endarterectomy
ABCD2 score: calculates the risk of a stroke/CV event following a TIA
Age >60
BP >140/90
Clinical features: unilateral weakness (2)/speech disturbance (1)
Duration of symptoms: >1hr (2), 10-59mins (1)
Diabetes?
Define MS and the 4 subtypes of MS
Inflammatory plaques of demyelination in the CNS
Defined as 2 episodes of neurological dysfunction separated in time and space (>30 days apart, in multiple body sites)
May be clinical isolated (episodes of neurological dysfunction due to CNS inflammation but no radiological signs) or radiologically isolated (classical MS presentation on scans but no clinical/physical signs)
- primary progressive
- secondary progressive
- relapsing remitting
- progressive relapsing
What is the pathophysiology of MS?
cause unclear, genetics + environment (EBV, smoking, low sunlight/vit D)
leads to autoimmune mediated CNS demyelination, demyelinated areas undergo inflammation and heal poorly leading to axonal damage and loss of neurological function
What are the signs/symptoms of MS?
CNS that is affected therefore UMN signs!
Cognitive -> amnesia, poor mood, poor executive functioning
Motor -> transverse myelitis (weakness and sensory loss below level of lesion)
Sensory -> paraesthesia, reduced vibration, dyaesthesia
GI -> swallowing disorders, constipation
Eye -> optic neuritis (painful central field visual loss)
Cerebellum -> tremor, falls, limb ataxia
Bladder -> incontinence
What investigations should be carried out if MS is suspected and how is it diagnosed clinically?
Diagnosed clinically by 2 episodes of demyelination, disseminated in time and space:
Imaging
- MRI of brain/SC
Bloods
- FBC (exclude differentials like vitamin deficiencies, infections)
- TFTs
- VitB12 levels
- CSF (looks for oligoclonal Ig bands/cell count)
What are the treatments for MS?
1) lifestyle: smoking cessation, avoid stress, exercise
2) manage the acute episode: high dose STEROIDS +/- bone protection
3) Disease modifying treatment (to prevent relapses):
- Beta-interferon
- Dimethyl fumerate (reduces WCC)
- ALEmtuzumab (monoclonal AB)
- NATalizumab (monoclonal AB)
- Fingolimod (sequesters lymphocytes in LN’s to prevent them taking part in the immune response)
Define SAH and its causes
spontaneous bleeding into the subarachnoid space
can be traumatic or non-traumatic (e.g. intra-cranial aneurysm)
What is the pathophysiology of SAH?
What are the risk factors for an SAH?
80% due to aneurysm formation
20% due to neoplasia or arterio-venous malformation
aneurysm forms due to haemodynamic stress on the vessel and inflammatory changes, blood then seeps into the subarachnoid space
RFx: smoking, HTN, alcohol, FHx, ADPKD, previous aneurysm, co-arctation of aorta, CTD
What are the signs/symptoms of SAH?
thunderclap headache +/- sentinel preceeding headache N&V photophobia LOC seizures visual/speech/motor disturbances meningism
What investigations should be carried out if SAH is suspected?
Immediate CT
Bloods (FBC, coag, U&E, troponin)
ECG
LP -> only if diagnosis cannot be made from CT, and should be carried out 12hrs after the onset of headache to detect xanthochromia (yellow colour suggesting old blood present from a SAH), also red cell count of CSF
CT angiogram (would reveal any aneurysms)
Describe the WFNS grading system of SAH:
1 - GCS 15 -> no motor deficit 2 - GCS 13-14 -> no motor deficit 3 - GCS 13-14 -> motor deficit 4 - GCS 7-12 -> +/- motor deficit 5 - GCS 3-6 -> +/- motor deficit
How is SAH treated?
Aim = maintain cerebral perfusion and keep hydrated Obs: GCS, CT, pupils, BP Fluids to maintain cerebral perfusion Antiembolic stockings Nimodipine (ca channel blocker) Analgesia
Surgical options: surgical clipping (to exclude aneurysm from circulation) endovascular coil embolisation
What are the complications of SAH?
rehaemorrhage
DVT (as SAH induces a pro-thrombotic state)
Hyponatraemia
Hydrocephalus
Cardiopulmonary complications (MI, sudden arrhythmias, death)
Seizures
Delayed ischaemia
What are the red flags to check for when investigating a patient with a headache?
SNOOP-T Systemic symptoms? Neurological features? Older age of onset? Onset acute? Previous headaches? Trigger e.g. valsalva?
Describe ICP and the Monroe-Kellie hypothesis
Skull contains brain, blood and CSF
Monroe-Kellie hypothesis: an increase in 1 component leads to a decrease in one of the other 2 components
CPP = MAP - ICP
Describe a migraine and its investigation/treatment
Severe unilateral, throbbing headache Usually episodic with triggers (CHOCOLATE) - caffeine - hangovers - orgasms - cheese/chocolate - OCP - lie ins - alcohol - travel - exercise pt likes to curl up in quiet room usually: prodrome with aura (30%) = visual changes Management: - lifestyle: avoid triggers - prophylaxis: B-blockers, TCA, topiramate - during attack: analgesia, triptans, antiemetics
Describe a cluster headache and its investigation/treatment
unilateral severe pain
usually felt around the eyes with: lacrimation, conjuctivitis, rhinorrhoea, Horner’s syndrome
common in middle aged men
?stress related
S/Sx: lasts 10 mins - 1 hr, usually 1-3x a day in clusters which last weeks/months
may be early morning and awake pt from sleep
patient WILL WANT TO PACE AROUND
Management in attack:
- triptans (5-HT serotonin agonists)
- oxygen
- steroids
Preventative:
- verapamil
- steroids
Describe a tension headache and its investigation/treatment
diffuse, dull, band like headache \+/- scalp tenderness usually self-limiting aggravated by noise/light lasts hrs/days varying frequency
No abnormal physical signs
Tx: reassure patient that a sinister cause is unlikely, give analgesia/TCA’s for prophylaxis
NOTE: these headaches can be exacerbated by analgesia over-use so wean off opiates if the patient presents with analgesic/tension headache
Describe a thunderclap headache and its investigation/treatment
abrupt onset of severe headache in <5mins and lasting >1hr
SAH until proven otherwise
Described as being hit over head
Describe a low pressure headache and its investigation/treatment
Due to CSF leakage, the loss of CSF volume causes traction on the meninges/cranial nerves
Can occur:
- post LP
- with a dural tear
- post-valsalva
Better when lying down and worse sitting up
Describe a high pressure headache and its investigation/treatment
headache due to pressure on pain-sensitive brain structures - can cause N&V, HTN, respiratory changes and increased HR Causes: - aneurysm, tumour, brain injury, encephalitis, hydrocephalus, HTN, meningitis, stroke - worse when lying down and better when standing - worse on exertion/valsalva other signs: - visual changes - papilloedema - enlarged blind spot - 3/6th CN palsies - N&V - meningism
Define Parkinson’s disease and Parkinsonism
Parkinsonism = bradykinesia + 1 of: tremor, rigidity or postural instability
Parkinson’s disease = parkinsonism due to formation of Lewy bodies in basal banglia, and loss of dopaminergic neurons in the substantia nigra
What is the pathophysiology of Parkinson’s disease?
mainly sporadically caused by there are some genetic links (LRRK2)
Due to loss of dopaminergic neurons in the midbrain (in substantia nigra)
The surviving neurons contain misfolded a-synuclein protein in their nucleus called lewy bodies -> why these form is unclear but thought to be due to inflammation, apoptosis, infection, oxidative stress, mitochondrial dysfunction
What are the S/Sx of PD (motor and non-motor)?
Motor:
- cogwheel rigidity
- postural instability
- resting/pill-rolling tremor
Non motor: (NASO)
- Neuropsychiatric: dementia, depression, anxiety
- Autonomic: constipation, sweating, urinary urgency, postural hypotension
- Sleep (REM behaviour)
- Other (fatigue, pain/sensory symptoms, reduced olfactory function)
How is PD diagnosed?
Mainly a clinical diagnosis
Imaging: CT (usually NORMAL but used to rule out other causes)
Functional imaging: DATSCAN injection (radioactive tracer with high affinity for DAT dopamine transporter on dopaminergic neurons with PET scan)
Bloods: exclude other causes e.g. TFT, copper
What are the treatment options for PD?
Focus on symptom control and halting disease progression
1) Pharmacological:
- levodopa
- carbidopa
- pramipexole/ropinirole
- apomorphine
- orphenadrine/benzhexol
- selegiline/rasagiline
- entacapone/tolcapine
2) Non pharmacological:
- DBS
- surgical ablation of overactive basal ganglia
- MDT!
What is the definition of cervical spondylosis?
Degeneration of the cervical spine, inevitable with age
Has widespread clinical spectrum ranging from asymptomatic -> progressive spastic quadriparesis
Due to compression of the spinal cord
What are the causes of cervical spondylosis and its S/Sx?
Due to degeneration of the annulus fibrosis (surrounds nucleus pulposus) + thickened ligamentum flavum posteriorly leads to narrowing of the spinal canal and intervertebral foramina
= the spinal cord is then dragged over bony spurs as the neck flexes and extends
S/Sx:
- neck stiffness
- Lhermitte’s sign = neck flexion which produces tingling down the spine
- nerve root impingement
- features of cord compression: weakness, clumsy hands/gait disturbance/incontinence/hesitancy/urgency
What are the red-flag features of back pain?
MMAYFINS! malignancy history morning stiffness acute onset young age of onset fever/night sweats/weight loss immunosuppression neuro symptoms/nocturnal pain sphincter disturbance
How is cervical spondylosis investigated and treated?
MRI/CT Specialist referral Analgesia Encourage gentle activity Surgery -> cervical epidural, transforaminal injections -> surgical decompression
Describe myasthenia gravis and its aetiology
A chronic autoimmune disorder where autoantibodies are made against the ACh receptor at the post-synaptic junction
These autoantibodies prevent ACh binding to the post-synaptic junction receptors and mean that action potential are not transmitted through nerves
What are the signs/symptoms of myasthenia gravis?
Associated with thyomas/thymic hyperplasia
Muscle weakness which worsens with exercise and improves with rest
Fatiguable muscle weakness: extraocular, bulbar, neck, respiratory and then limbs affected
Signs:
ptosis, diplopia, peek sign (tight closing of the eyelids can cause muscle fatigue and result in the white of the sclera slowly becoming apparent under the partially opened eye), voice fades as counting up to 50
What investigations should be carried out for myasthenia gravis?
Bloods: anti-AChR antibodies, muscle specific antibodies?
Electromyography: decrimental response to repetitive nerve stimulation
Imaging: CT to exclude thyoma
Other: eg. applying ice to the eyelids will improve ptosis
What is the treatment for myasthenia gravis?
1) Acutely: IV immunoglobulins Plasma exchange 2) Long term: Pyridostigmine (anticholinesterase inhibitor) Steroids Thymectomy
Define MND:
cluster of neurodegenerative diseases caused by loss of UPPER AND LOWER motor neurons in the SC/CN’s and spinal cord
- NO SENSORY LOSS (different to MS) and NO EYE CHANGES (different to Myaesthenia Gravis)
Describe the 4 categories of MND:
1) Amylotrophic lateral sclerosis (MND) = 80%
- loss of neurons in the motor cortex and anterior horn of the SC, presents with UMN and LMN signs
2) Progressive bulbar palsy = 10-20%
- affects CN9-11
- affects tongue, swallowing and speech
3) Progressive muscular atrophy = <10%
- anterior horn cell lesion
- LMN signs only
- weakness/wasting of distal limb muscles
4) Primary lateral sclerosis (rare)
- UMN signs only, loss of Betz cells in motor cortex, no cognitive decline
Describe the signs and symptoms of MND:
UMN signs:
- spasticity
- brisk reflexes
- up going plantars
LMN signs:
- muscle wasting
- fasciculations
Bulbar signs:
- speech/swallowing difficulties
25% have fronto-temporal dementia
Think: stumbling gait, foot drop, proximal myopathy, weak grip (door handles/buttons), aspiration pneumonia, weak shoulder abduction (hair washing hard!)
What investigations should be carried out to diagnose MND and what criteria is used?
El-Escorial criteria: based on the number of UMN/LMN signs which gives a definite/probable/suspected category to the diagnosis
- Clinical diagnosis
- Bloods: may be normal, mildly raised CK, VitB12, ?genetic testing, ?antibodies
- Electromyography (can confirm nerve damage)
- MRI (?spinal root compression may resemble ALS)
What are the treatment options for MND?
No good treatments!
Non-invasive ventilatory support/percutaneous feeding may increase quality of life for some patients
MDT:
- OT, PT, speech therapist, dietician, neurologist, palliative teams
What is the definition of a peripheral neuropathy and what are the 4 types?
Nerve dysfunction affecting the PNS (all nerves except brain and SC)
1) length dependent neuropathies
2) Guillain barre syndrome
3) mononeuropathies
4) myaesthenia gravis
Describe upper motor neuron lesion signs:
Little muscle wasting
Increased tone and spasticity
Hyper-reflexia
Primitive reflexes (upgoing plantars/+ babinski sign)
Describe lower motor neuron lesion signs:
Muscle wasting/atrophy
Flaccid/normal muscle tone
Hypo/areflexia
Fasciculations
Describe the MRC grading system for power of muscles:
0 = no muscle contraction 1 = flickers of contraction but no movement 2 = some movement but cannot overcome gravity 3 = movement which can overcome gravity but not resistance 4 = movement but reduced power against resistance 5 = normal muscle power and movement
Describe length-dependent neuropathies and their causes:
Due to axonal (not myelin) changes = causing slower nerve conduction
- Distal symptoms (hand/feet weakness/numbness)
- seen in: DM, B12/folate deficiency, alcohol, neoplastic
Describe Guillain-Barre syndrome and its causes/presentation:
Post-infectious aetiology
Autoimmune
Immune cells attack myelin sheath on nerves causing demyelination and progressive muscle ascending weakness over days
Sensory and motor neurones involved
What is meningism?
neck stiffness, photophobia, headache, kernigs sign +
What is kernigs sign?
Flex hip and knee at 90 degrees
Then extend the knee and this causes pain indicating SAH/meningitis
What are the differentials of a subarachnoid haemorrhage?
Headache - migraine Meningitis Intracerebral bleed Carotid/vertebral artery dissection Benign thunderclap headache -> can be triggered by valsalva, cough, coitus
What are the 4 subtypes of MS
1) Primary progressive -> constantly getting worse, no plateau periods
2) relapsing remitting -> relapses with period of no progression in between
3) secondary progressive -> begins are (2) but then there are no relapses and symptoms get progressively worse
4) Progressive relapsing -> steadily worsening function with occasional relapses
When are triptans contraindicated in migraine treatment?
Triptans are contraindicated in CVD/HTN (as they can increase BP)
What is subacute degeneration of the spinal cord?
Motor and sensory nerves become damage due to vitamin B deficiency (leads to loss of fatty myelin sheath)
You should always replace B12 > folate (as replacing folate when B12 is low can exacerbate B12 deficiency, the mechanisms by which it does this are unclear)
What things can exacerbate the features of myaesthenia gravis?
pregnancy infection exercise drugs - gentamicin - opiates - B blockers - tetracyclines
What can an overdose of pyridostigmine (and
other anticholinergics) cause?
Muscle fasciculations Pallor Sweating XS salivation Small pupils
Define parkinsonism
Parkinsonism = Bradykinesia + one of: rigidity, rest tremor + postural instability
Compare and contrast Parkinson’s tremor vs Essential tremor
Parkinson's: 4-6Hz Unilateral Improves with movement, worse with rest No change with alcohol
Essential tremor: 6-8Hz (faster) Symmetrical Worse with movement and improves with rest Improves with alcohol
What is the treatment for tonic clonic seizures?
1st - sodium valproate
2nd - lamotrigine/carbemazipine
What is the treatment for focal seizures?
(Opposite to tonic clonic)
1st - lamotrigine/carbemazipine
2nd - sodium valproate
What is the treatment for absence seizures?
Sodium valproate/Ethosuxsamide
What is the treatment for atonic and myoclonic seizures?
1st line - Sodium valproate
2nd line - Lamotrigine
What are the 4 ways in which sensation is tested in a neurological examination, and which pathways convey each?
1) Pinprick (pain) = spinothalamic
2) light tough (dorsal column)
3) Vibration (dorsal column)
4) Proprioception (dorsal column)
What is Brown Sequard syndrome?
A unilateral spinal cord lesion
On the IPSILATERAL side to the lesion is causes loss of motor supply (paralysis) and loss of proprioception, vibration and light touch
On the CONTRALATERAL side to the lesion it causes loss of pain and temperature
Describe the nerve pathways behind an RAPD
Light shone into one eye (CN2) causes stimulation of BOTH the Left and Right Eddinger-Westphal nuclei in the brain.
EW nuclei then send out action potentials down both CN3 to cause constriction of both pupils!
What nerve root controls shoulder abduction
C5
What nerve root controls elbow flexion
C5
What nerve root controls elbow extension
C7
What nerve root controls wrist extension
C6
What nerve root controls finger abduction
T1
What nerve root controls finger flexion
C8
Name the nerve roots involved in the
a) biceps
b) supinator
c) triceps reflexes?
a) biceps = C5/6
b) supinator = C4/6
c) triceps = C7
What nerve root controls hip flexion
L2
What nerve root controls knee extension
L3
What nerve root controls ankle dorsiflexion
L4
What nerve root controls ankle plantarflexion
S1
What nerve root controls big toe extension
Purely L5
What nerve root controls patellar reflex
L3,4 kick the door
What nerve root controls ankle reflex
S1,2 buckle my shoe
List side effects of lamotrigine
Can cause Steven-Johnson syndrome (blistering skin disease) -> ESPecially when lamotrigine is given with sodium valproate, as sodium valproate is an enzyme inhibitor!
List side effects of carbemazipine
Agranulocytosis
Dizzy
Ataxia
(is a P450 enzyme inducer - therefore careful in concurrent contraceptive use!)
List side effects of sodium valproate
- P450 enzyme inhibitor, therefore can increase the potency of other drugs Also: - TERATOGENIC! - allopecia - tremor - hepatotoxic
Compare the provoking factors for a seizure vs syncope
Seizure triggers: drugs, sleep deprivation, visual stimuli
Syncope triggers: low BP, heat, dehydration
Describe the background, prodrome, event and post-drome of a non-epileptic attack
Background: anxiety, depression, sexual/physical abuse
Prodrome: non-specific, breathing difficulties
Event: tremor all over, back arching, resisted eye opening
After event: retains memory of the event, emotional, tearful, rapid recovery
List the parkinson’s plus syndromes
Parkinson plus disorders: can mimic Parkinson’s but do not respond to the medications, and have a different disease trajectory
1) MSA - multiple systems atrophy
2) Dementia with Lewy bodies
3) PSP - progressive supranuclear palsy (causes a vertical gaze palsy)
4) CBD - corticobasal disease
Describe MSA
MSA - multiple systems atrophy
- This is a rare condition where the neurones of multiple systems in the brain degenerate.
- It affects the BASAL GANGLIA as well as multiple other areas.
- The degeneration of the basal ganglia lead to a Parkinson’s presentation.
- The degeneration in other areas lead to autonomic dysfunction (causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).
Describe the key features of PSP
Causes a vertical gaze palsy
