Neuro Flashcards
What is the pathophysiology of multiple sclerosis
acquired chronic immune mediated inflammatory condition of the CNS.
autoimmune destruction of oligodendrocytes by T cells
demylination
gliosis - scarring
neuronal damage leading to cell loss
What are the different types of MS
relapsing remitting
secondary progressive
primary progressive
Describe the course of relapsing remitting MS
symptoms come and go. Periods of good health or remission are followed by sudden symptoms or relapses
Describe the course of secondary progressive MS
the onset of MS is of the RRMS pattern. But, at some point later, the disease course changes and neurological function gradually worsens, with or without continued relapses.
Describe the course of primary progressive MS
from the beginning, symptoms gradually develop and worsen over time
Define a relapse in MS
onset of new or worsening of current symptoms
attributable to demyelinating disease
>24hr onset
absence of infection, fever, metabolic disturbance
What are the most common presentations of MS
optic neuritis - partial or total unilateral visual loss, pain on movement, dereased visual acuity, decreased colour sensitivity
transverse myelitis - paresthesia or weakness below level of inflammation
cerebellar problems - ataxia, vertigo, clumsiness, dysmetria
brain stem problems - ataxia, abnormal eye movements, dysphagia
What is Lhermitte’s phenomena
shock like sensation radiating down the spine induced by neck flexion
Give some differentials for MS
neuromyelitis optica low vit B12 Lyme disease tertiary syphilis HIV SLE sarcoidosis brain neoplasm
What is the key diagnostic investigation in MS
MRI head - periventricular lesions and discrete white matter abnormalities
What is the treatment for a relapse of MS
IV or oral steroids - metyhlprednisolone for 5 days
What is the treatment long term for MS
DMARDs - eg. interferon beta
management of long term problems of fatigue, pain etc
What causes a seizure
neurons synchronously depolarising due to increased excitation or decreased inhibition
What are the main excitatory and inhibitory neurotransmitters in the brain
excitatory: NMDA
inhibitory: GABA
Define seizure
transient occurrence of signs and symptoms due to abnormal electrical activity in the brain
What is the difference between a partial seizure and a generalised seizure
partial - only part of the brain is affected
generalised - both hemispheres affected
What is the difference between a simple partial seizure and a complex partial seizure
partial - no loss of consciousness, remember what happened
complex - partial or complete loss of consciousness, may not remember it
What is a secondary generalised seizure
started as partial, becomes generalised
What happens in a tonic seizure
become stiff, flexed. fall backwards
What happens in an atonic seizure
become relaxed, complete loss of tone, fall forwards
What happens in a clonic seizure
convulsions
What happens in a tonic-clonic seizure
increased tone and convulsions
What happens in a myoclonic seizure
short muscle twitches
What happens in an absence seizure
lose and regain consciousness, zones out
What is a Jacksonian march
seizure starts in small area eg hand, then spread to larger eg arm. Can become generalized
What are some of the signs or symptoms of post-ictal period
Drowsiness or amnesia.
Injury, including bites to the sides of the tongue.
Aching limbs or headache.
Focal neurological deficit, that slowly recovers.
What is Todd’s paralysis
a focal neurological deficit, most commonly weakness, that occurs after a seizure
fully recovers after 48 hours
How is epilepsy defined
At least two unprovoked seizures occurring more than 24 hours apart.
One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures, occurring over the next 10 years.
Diagnosis of an epilepsy syndrome — there are at least 30 different epilepsy syndromes distinguished by their seizure type, age of onset, family history, neurological findings, cerebral imaging (such as CT or MRI scan), electroencephalogram (EEG) pattern, and underlying cause.
What are the causes of epilepsy
idiopathic cerebrovascular disease cerebral tumour post traumatic fetal hypoxia or trauma cortical or vascular malformation cerebral abscess epilepsy syndromes
What are the differential diagnoses for a seizure
What would help you rule these in/out
syncope - postural change, pale. Feel faint/lightheaded beforehand, blurred vision, ringing ears
arrhythmia - prev IHD/SHD, palpitation, breathless, CP
hyperventilation of anxiety - fear, breathless, paresthesia
febrile convulsions - temp >37.8, 6m-5y
alcohol withdrawal - known alcoholic, around 36 hours following cessation of drinking
infantile spasms - flexion of head, trunk and limbs, extension of arms
Psychogenic non-epileptic seizures - history of mental health problems or a personality disorder
What investigations need to be done in a patient presenting with a seizure
obs, LSBP, ECG
glucose, U+E
EEG, MRI
What is the definition of status epilepticus
continuous seizure for 30 minutes or longer,
or recurrent seizures without regaining consciousness lasting 30 minutes or longer.
What is the emergency treatment for a seizure
<5mins
Protect them from injury by:
Cushioning their head with your hands or soft material.
Removing harmful objects from nearby
Do not restrain them or put anything in their mouth.
When the seizure stops, check their airway and place them in the recovery position.
Observe them until they have recovered.
Examine for, and manage, any injuries.
Arrange emergency admission if it is their first seizure.
> 5mins or more than 3 in 1hr
Buccal midazolam as first-line treatment or rectal diazepam
Intravenous lorazepam if intravenous access is already established and resuscitation facilities are available.
Phenytoin after 20 mins
When should an ambulance be called for someone having a seizure
if seizures do not respond promptly to treatment.
Seizures were prolonged or recurrent before treatment was given, particularly if seizures had developed into status epilepticus.
There is a high risk of recurrence, such as a history of repeated seizures or status epilepticus.
There are difficulties monitoring the person’s condition.
This is their first seizure.
What is the first line management of generalised seizures
sodium valproate
or ethosuximide in absence
What is the second line management for generalised seizures?
lamotrigine
myoclonic: levetiracetam or topiramate
tonic/atonic: lamotrigine as adjunctive
What is the first line management of partial seizures
lamotrigine or carbemazepine
What is the second line management of partial seizures
levetiracetam, carbemazepine or sodium valproate
When can one consider stopping antiepileptic drugs?
if seizure free for >2 years
stop gradually over 2-3 months
What are the key side effects of lamotrigine
Stevens-Johnson syndrome
What are the indiations for starting AEDs
second seizure
the patient has a neurological deficit
brain imaging shows a structural abnormality
the EEG shows unequivocal epileptic activity
the patient or their family or carers consider the risk of having a further seizure unacceptable
What is the pathophysiology behind alcohol withdrawal seizures
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.
Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission), therefore leading to over excitation
What are the key side effects of sodium valproate
increased appetite and weight gain alopecia: regrowth may be curly P450 enzyme inhibitor ataxia tremor hepatitis pancreatitis thrombocytopaenia teratogenic (neural tube defects)
What are the key side effects of carbemazepine
P450 enzyme inducer - decreases effectiveness of contraceptives
dizziness and ataxia
drowsiness
leucopenia and agranulocytosis
SIADH
visual disturbances (especially diplopia)
Which contraceptives are recommended to take whilst on carbemazepine?
Why is this?
copper IUD
mirena
depo-provera injection
not metabolised by P-450
What advice is given to patients with epilepsy during pregnancy
risks of uncontrolled epilepsy during pregnancy generally outweigh the risks of medication to the fetus.
All women thinking about becoming pregnant should be advised to take folic acid 5mg per day well before pregnancy to minimise the risk of neural tube defects.
lamotrigine
decreased risk of teratogenicity
What advice is given to patients with epilepsy who drive
need to inform DVLA
cannot drive for 6 months following a seizure.
must be fit free for 12 months before being able to drive if they have established epilepsy
Is breast feeding safe whilst taking AEDs
yes
although not with barbiturates
What is motor neruone disease
group of disordrs characterised by progressive paralysis due to anterior horn cell and motor cranial nuclei damage
leads to LMN and UMN dysfunction
What age group is MND most common in
43-52 years in familial
58-63 years in sporadic
What are the features of MND
limbs: dropping objects, fasciculations, NO SENSORY SIGNS, wasting of hand muscles, weakness and cramping
bulbar: slurring, tongue fasciculations and wasting, dysphagia, emotional lability
resp: dyspnoea, orthopnoea, waking from sleep
What is a stroke?
a sudden interruption of blood supply to the brain
What is the difference between an ischaemic and haemorrhagic stroke
Ischaemic: obstruction within blood vessels preventing blood flow to the brain,
Haemorrhagic stroke: blood vessel ruptures reducing blood flow to the brain
What is the difference between an ischaemic stroke and a TIA
stroke: obstruction within blood vessels preventing blood flow to the brain, lasting >24 hours
TIA: obstruction within blood vessels preventing blood flow to the brain, lasting <24 hours
What is the difference between a thrombotic and embolic stroke
Thrombotic - Thrombus from a large artery e.g. carotid
Embolic - Blood clot, fat, air or bacterial embolus. AF can cause
What are the risk factors for stroke (including specific for ischaemic and haemorrhagic)
Non-specific: • Age • HTN • Smoking • Hyperlipidaemia • Diabetes • Alcohol • Medications • Genetics • Obesity • Sedentary lifestyle
Ischaemic stroke:
• AF
Haemorrhagic stroke:
• Anticoagulation therapy
• Arteriovenous malformation`
What do the parietal lobes do
- Communication with other lobe
- Perception
Dominant hemisphere
- Understanding the world
- Maths
- Language
Non-dominant hemisphere:
- Visuospatial functions
What do the frontal lobes do
- Higher level cognition (executive functioning)
- Thinking
- Planning
- Organising and problem solving
- Emotions
- Behaviour control
- Personality
- Broca’s area in dominant = Produce speech
What do the occipital lobes do
- Visual processing
What do the temporal lobes do
- Auditory processing
- Primary auditory cortex
- Wernicke’s in Left temporal lobe = Understanding Language
- Memory
What does the cerebellum do
- Balance
- Movement
- Coordination
What does the brainstem do
- Involuntary actions
- Heart rate
- Breathing
- Blood pressure
- Swallow
- Regulates hormones
Which parts of the brain do the anterior cerebral arteries supply
most midline portions of the frontal lobes
superior medial parietal lobes.
Which parts of the brain do the middle cerebral arteries supply
lateral surface of the hemisphere;
lateroinferior frontal lobe (location of Broca’s area i.e. language expression)
lateral temporal lobe (location of Wernicke’s area i.e. language comprehension)
What parts of the brain do the posterior cerebral arteries supply
cerebellum
occipital lobe
What are the three signs that the OXFORD (Bamford) STROKE CLASSIFICATION use to classify strokes
- unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
- contralateral homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
What causes a TACI (total anterior circulation) and what are the symptoms
- Middle and Anterior Cerebral arteries
- All 3 criteria are present
(1. unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. contralateral homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia)
What causes a PACI (partial anterior circulation) and what are the symptoms
- Smaller arteries of the Anterior Circulation e.g. Upper or Lower division of Middle Cerebral artery
- 2 criteria are present
(1. unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. contralateral homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia)
What causes a POCI (posterior circulation) and what are the symptoms
• Vertebrobasilar arteries
Presents with 1 of:
• Cerebellar or brainstem syndromes
• Loss of consciousness
• Isolated homonymous hemianopia
What causes a LACI (lacunar circulation) and what are the symptoms
• Perforating arteries around internal capsule, thalamus and basal ganglia
Presents with 1 of: • Pure unilateral motor dysfunction of face and arm, arm and leg or all 3. • Pure sensory stroke • Mixed motor and sensory • Ataxia: ataxic hemiparesis
What causes a LACI (lacunar circulation) and what are the symptoms
• Perforating arteries around internal capsule, thalamus and basal ganglia
Presents with 1 of: • Pure unilateral motor dysfunction of face and arm, arm and leg or all 3. • Pure sensory stroke • Mixed motor and sensory • Ataxia: ataxic hemiparesis
What problems does a lesion in the anterior cerebral artery cause
Contralateral hemiparesis and sensory loss,
lower extremity > upper (midline does lower extremities)
What problems does a lesion in the middle cerebral artery cause
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
What problems does a lesion in the posterior cerebral artery cause
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
What problems does a lesion in the posterior inferior cerebellar artery cause
Ipsilateral: facial pain and temperature loss (sensory)
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
What problems does a lesion in the anterior inferior cerebellar artery cause
Ipsilateral: facial pain and temperature loss (sensory)
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
also
Ipsilateral: facial paralysis and deafness
What problems does a lesion in the basilar artery cause
locked in syndrome
paralysis of body and facial muscles
consciousness and some eye movements are preserved
What causes Weber’s syndrome? What are the features?
lesion in branches of the posterior cerebral artery that supply the midbrain
Ipsilateral CN III palsy - down and out
Contralateral weakness of upper and lower extremity
How should an ischaemic stroke be managed immediately?
- A to E assessment
- Ensure the following parameters are normal:
Blood glucose
Hydration
Oxygen saturation
Temperature - Do not try and lower blood pressure in the acute phase
- Aspirin 300mg PO/rectally as soon as haemorrhagic stroke excluded
- Statin if cholesterol > 3.4mmol/L (wait for 48 hours)
- Thrombolysis with Alteplase if:
Able to be administered within 4.5 hours of onset of symptoms
Exclusion of haemorrhagic stroke by imaging
- Carotid endarterectomy if carotid territory and no severe disability *
What drugs are used for long term secondary prevention after an ischaemic stroke
first line: clopidogrel
second line: aspirin plus MR dipyridamole if clopidogrel is contraindicated or not tolerated,
third line: MR dipyridamole alone only if aspirin or clopidogrel are contraindicated or not tolerated
How should a TIA be managed
- Aspirin 300mg immediately (unless contraindicated due to bleeding disorder or already taking anticoagulant)
- Refer to specialist
What are the absolute contraindications to thrombolysis in an ischaemic stroke
- Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or traumatic brain injury in preceding 3 months
- Lumbar puncture in preceding 7 days
- Gastrointestinal haemorrhage in preceding 3 weeks
- Active bleeding
- Oesophageal varices
- Pregnancy
- Uncontrolled hypertension >200/120mmHg
What are the relative contraindications to thrombolysis
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis - unusual susceptibility to bleed (hemorrhage) mostly due to hypocoagulability
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in preceding 2 weeks
How should a haemorrhagic stroke be treated?
- Consult neurosurgery
- Stop anticoagulants and antithrombotics
- Reverse anticoagulation ASAP
Warfarin: fresh frozen plasma
Heparin: Protamine Sulfate - Some trials have shown benefit to acutely lowering the BP
What is the ROSIER score used for?
assess likelihood of stroke
How is the ROSIER score calculated
Exclude hypoglycaemia first, then assess the following:
Lose a point for each of:
• Loss of consciousness or syncope
• Seizure activity
Gain a point for each of: • Asymmetrical facial weakness • Asymmetrical arm weakness • Asymmetrical leg weakness • Speech disturbance • Visual field defect
What is the advice regarding driving after a Stroke/TIA
1 month off driving, may not need to inform DVLA if no residual neurological deficit
What is cauda equina syndrome
compression of the cauda equina, the nerve roots caudal to the level of spinal cord terimination
What can cause cauda equina syndrome
Herniation of a lumbar disc - L4/L5 and L5/S1 level.
Tumours: metastases, lymphomas, spinal tumours.
Trauma.
Infection, including epidural abscess.
Congenital - eg, congenital spinal stenosis, kyphoscoliosis and spina bifida.
Spondylolisthesis.
Late-stage ankylosing spondylitis.
Postoperative haematoma.
Following spinal manipulation.
Inferior vena cava thrombosis.
Sarcoidosis.
What are the features of cauda equina syndrome
back pain- sudden onset urinary retention problems initiating urination or stopping stream lower limb sensory or motor deficit loss of reflexes at affected nerve root saddle/perianal paraesthesia constipation or incontinence reduced anal tone sexual dysfunction
What investigaitons need to be done urgently in cauda equina syndrome
MRI spine
How is cauda equina syndrome managed
urgent spinal decompression surgery!!!
Anti-inflammatory agents if inflammatory cause - eg, ankylosing spondylitis.
Infection causes should be treated with appropriate antibiotic therapy.
Spinal neoplasms should be evaluated for chemotherapy and radiation therapy.
Explain the difference between paraparesis, hemiparesis, monoparesis and quadraparesis
para = partial paralysis of the lower limbs
hemi - partial weakness on one side of the body.
mono = paresis of one limb due to due to a small infarction in the contralateral motor cortex.
quadra = all four limbs, usually as the result of injury to the spine.
What sensory level is the umbilicus at
T10
What sensory level is the nipple at
T4
What is the function of the corticospinal tract
voluntary motor control of body and face
Describe the route of the corticospinal tract
internal capsule
medulla - decussates here
travels in anterolateral spinal cord
State the location in the spinal cord, blood supply and level of decussation of the corticospinal tract
anterolateral spinal cord
anterior spinal artery
decussates at the pyramids of the medulla
What is the function of the lateral spinothalamic (part of the anterolateral system) tract
pain and temperature sensation
State the location in the spinal cord, blood supply and level of decussation of the lateral spinothalamic tract
anterolateral spinal cord
anterior spinal artery
decussates at or within an few segments of level of entry to the cord
What would a lesion to the lateral spinothalamic tract in the cord cause
contralateral loss of pain and temperature perception below level of lesion
State the location in the spinal cord, blood supply and level of decussation of the dorsal column medial lemniscus tract
posterior spinal cord
posterior spinal artery
decussates at medulla oblongata
What is the function of the DCML tract
sensation of proprioception and fine touch
What would a lesion to the DCML tract in the cord cause
ipsilateral loss of fine touch and proprioception sensation below level of lesion
What is Brown-Sequard syndrome and what does it cause?
hemisection (one sided lesion) of the spinal cord.
DCML pathway – ipsilateral loss of touch, vibration and proprioception.
Anterolateral system – contralateral loss of pain and temperature sensation.
It will also involve the descending motor tracts, causing an ipsilateral hemiparesis.
What causes Horner’s syndrome
disruption of tthe sympathetic nerves anywhere along their course -
Describe the course of the sympathetic nerve fibres to the eye
First-order sympathetic fibres originate in the hypothalamus and descend through the brainstem to level C8-T2 of the spinal cord where they synapse on preganglionic sympathetic nerve fibres.
Second-order fibres leave the cord at level T1 and ascend in the sympathetic chain over the apex of the lung to synapse in the superior cervical ganglion at the level of the bifurcation of the common carotid artery (C3-C4).
Third-order (postganglionic) fibres pass alongside the internal carotid artery, sending branches to the blood vessels and sweat glands of the face, and pass via the cavernous sinus to enter the eye via the superior orbital fissure. They pass via the long ciliary nerves to supply the iris dilator and Müller’s muscle (superior tarsal muscle)
What are the key features of horner’s syndrome
partial ptosis
miosis
hemifacial anhidrosis
What are the symptoms of horner’s syndrome
asymptomatic! partial ptosis miosis hemifacial anhidrosis facial flushing - if pre-glanglionic orbital pain/headache - if post-ganglionic
What should be examined in horner’s syndrome
Constricted pupil on the affected side -
Shine a torch in the eye to make the pupil constrict.
Remove the torch and watch the pupil dilate - the affected pupil lags behind the other in dilation
Ipsilateral dry skin on the face due to loss of sweating:
Ipsilateral partial ptosis
There is increased amplitude of accommodation - can focus on nearer objects more easily
Heterochromia irides may occur with congenital Horner’s syndrome - the iris on the affected side remains blue whilst the other changes to brown.
Examine for the presence of lymphadenopathy
What are the causes of Horner’s syndrome
central:
cerebrovascular accident
MS
preganglionic: Pancoast tumour lymphoma TB causing lymphadenopathy aortic or common carotid artery dissection trauma
Postganglionic
HSV
internal carotid artery dissection
How can the location of the lesion in Horner’s syndrome be determined clinically
the extent of the anhidrosis
if central: anhidrosis of face, arm adn trunk
if preganglionic: anhidrosis of face
if post ganglionic: no anhidrosis
What investigations should eb done in Horner’s syndrome
CXR
CT/MRI head
CT angiogram
What are some important questions to ask in a headache history? Why?
Site -
• Unilateral headache and eye pain—cluster headache, acute glaucoma
• Unilateral headache and ipsilateral symptoms—migraine, tumour, vascular
Quality -
• First and worst headache—subarachnoid haemorrhage
• Thunderclap headache—subarachnoid haemorrhage
Timing
• Worse in the morning or bending forward—↑icp/venous thrombosis
• Change in the pattern of ‘usual headaches’.
• Where have you been? - Malaria
Aggravating -
• Cough-initiated headache—↑icp/venous thrombosis
Secondary symptoms
• Persisting headache ± scalp tenderness in over-50s—giant cell arteritis
• Headache with fever or neck stiffness—meningitis
• Might you be pregnant? - pre-eclampsia
What do teh flexor and extensor response to pain show?
Flexion = decorticate posture (arms bent inwards on chest, thumbs tucked in a clenched fist, legs extended) implies damage above the level of the red nucleus in the midbrain.
• Extension = decerebrate posture (adduction and internal rotation of shoulder, pronation of forearm) indicates midbrain damage below the level of the red nucleus.
What are the features needed for a diagnosis of migraines
5 attacks
• Lasting 4 hours – 3 days
• 2 of unilateral, pulsating, severe affecting life
• 1 of N+V, photophobia, phonophobia
