Neurology Flashcards
(pronounced ghee-yan bar-ray)
Define Guillain-Barré syndrome? Summary of how it presents?
Pathophysiology?
2 Key features in the presentation?
How is diagnosis made? 3
Management? - 2 key things
Guillain-Barré syndrome is an acute paralytic polyneuropathy that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms.
^^^ If you didnt get this repeat the card!
It is usually triggered by an infection and is particularly associated with to Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the triggering pathogen. These antibodies also match proteins on the peripheral neurones. They may target proteins on the myelin sheath or the nerve axon itself.
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The characteristic features are:
Symmetrical ascending weakness
Reduced reflexes
extra: There may be peripheral loss of sensation or neuropathic pain. It may progress to the cranial nerves and cause facial weakness. Autonomic dysfunction can lead to urinary retention, ileus or heart arrhythmias.
Symptoms usually start within four weeks of the triggering infection. They begin in the feet and progress upward. Symptoms peak within 2-4 weeks. Then, there is a recovery period that can last months to years.
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Diagnosis
Clinical diagnosis based on the Brighton criteria (weakness, loss of reflexes…)
Ix that support the diagnosis:
- Nerve conduction studies (showing reduced signal through the nerves)
- Lumbar puncture for cerebrospinal fluid (showing raised protein with a normal cell count and glucose) -> dont fully get this because its a peripheral neuropathy?!
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Management:
VTE prophylaxis (pulmonary embolism is a leading cause of death)
IV immunoglobulins (IVIG) first-line
Plasmapheresis is an alternative to IVIG
Severe cases with respiratory failure may require intubation, ventilation and admission to the intensive care unit.
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Recovery can take months to years. Patients can continue regaining function five years after the acute illness. Most patients eventually make either a full recovery or are left with minor symptoms. Some are left with significant disability. Mortality is around 5%, mainly due to respiratory or cardiovascular complications.
Pathophysiology of Huntington’s:
Inheritence pattern? Gene and chromosome
Type of mutation?
What can happen to successive generations in families with huntington’s? Why is this?
Huntington’s disease (also called Huntington’s chorea) is an autosomal dominant genetic condition that causes progressive neurological dysfunction
It is a trinucleotide repeat disorder involving a genetic mutation in the HTT gene on chromosome 4, which codes for the huntingtin (HTT) protein.
Other examples of trinucleotide repeat disorders include:
Fragile X syndrome
Spinocerebellar ataxia
Myotonic dystrophy
Friedrich ataxia
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Anticipation
Huntington’s chorea displays something called genetic anticipation. Anticipation is a feature of trinucleotide repeat disorders, where successive generations have more repeats in the gene, resulting in:
Earlier age of onset
Increased severity of disease
TOM TIP: Anticipation is a common concept tested in exams and worth remembering with Huntington’s.
Huntington’s Chorea:
How does it present? X + 5+ movement disorders (name them)
Ix?
Management?
Prognosis and two key causes of death?
Pathophysiology is tested on another card.
Huntinton’s causes progressive neurological dysfunction
It typically begins with cognitive, psychiatric or mood problems, followed by the development of movement disorders:
- Chorea (involuntary, random, irregular and abnormal body movements)
- Dystonia (abnormal muscle tone, leading to abnormal postures)
- Rigidity (increased resistance to the passive movement of a joint)
- Eye movement disorders
- Dysarthria (speech difficulties)
- Dysphagia (swallowing difficulties)
Key - remember cognitive and behavoiral changes followed by movement disorder.
Me - for understnading not memeory - Huntingtin protein isnt well understood but known to play a role in the healthy functioning of neurones in the cortex and striatum (basal ganglia), hence why there is problems with controlling movement, cognition, and emotion.
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Ix- diagnosis is made by genetic testing
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Management:
There are currently no treatment options for slowing or stopping the progression of the disease.
- Tetrabenazine may be used for chorea
- SSRIs for depression
- physiotherapy to maintain mobility and prevent contractures, SALT to help with dysphagia and dysarthria
- Palliative care
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Life expectance is around 10-20 years after the onset of symptoms. As the disease progresses, patients become more frail and susceptible to illness (e.g., infections, weight loss, falls and pressure ulcers). Death is often due to aspiration pneumonia. (Dysphagia)
Suicide is also a common cause of death.
Subarachnoid Haemorrhage:
- what is the subarachnoid space?
- What is the main cause of a SAH
- How does a subarachnoid haemorrhage present? Sx in addition to headache?
Subarachnoid haemorrhage involves bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane.
This is usually the result of a ruptured cerebral aneurysm.
Subarachnoid haemorrhage has a very high mortality (around 30%) and morbidity, making it essential not to miss.
Presentation:
The typical history is a sudden-onset occipital headache during strenuous activity, such as heavy lifting or sex. The sudden and severe onset leads to the “thunderclap headache” description. It may feel like being struck over the back of the head.
Other important features include:
Neck stiffness - makes sense there is mengeal irriation, but the sudden vs gradual onset headache is the differenting factor i think
Photophobia
Vomiting
Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)
Subarachnoid Haemorrhage:
- 3 Investigations? What do they show?
- Management? Options for repair; drug used
- other key complication
Ix:
- First Line - CT head - shows hyperattenuation (white) in the subarachnoid space (basically in the fissures/sulci and the ventricles)
- Lumbar puncture: performed if the CT head appears normal (does not exclude SAH). Performed 12 hours after symptom onset to allow billirubin to accumulate in the CSF. Shows:
- Raised red cell count
- xanthochromia (yellow colour caused by billirubin)
CT angiography is used after confirming the diagnosis to locate the source of the bleeding.
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Management:
- intubation and ventilation if conciousness is reduced
- Surgical - repair of aneurisms - can be endovascular coiling or neurosurgical clipping - both cut the anuerism off from the artery
- Nimodipine (CCB) is used to prevent vasospasm (a common complication that leads to brain ischemia)
Complications:
Hydrocephalus (increased CSF - due blood clots obstructing outflow of CSF/absorbtion) is managed with lumbar puncture, external ventricular drain (in to a drainage bag externally) or a ventriculoperitoneal shunt (into peritoneal cavity).
Remember you can view card in deck for other info on subarachnoid haem
KEY NEUROANATOMY FOR INTRACRANIAL HAEMORRHAGES
Which blood vessels are found in each of the four spaces between the meninges?
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What are the layers of the BBB?
WARNING MADE WITH CHAT GTP BUT THINK IT IS ACCURATE, HELPFUL FOR SURE.
Epidural Space (Potential space between the skull and dura mater)
Vessels: Middle meningeal artery
The middle meningeal artery and other meningeal arteries run in the potential space between the skull and the dura mater. This space is generally “closed” unless there’s an injury.
Subdural Space (Potential space between the dura mater and arachnoid mater)
Vessels: Bridging veins
The bridging veins pass through the subdural space, connecting the superficial veins of the brain to the dural venous sinuses.
Side note for understanding: The dural venous sinuses are large venous channels located within the layers of the dura mater (the outermost layer of the meninges). These sinuses collect venous blood from the brain and cerebrospinal fluid (CSF) from the subarachnoid space and drain it into the internal jugular veins, which carry the blood back to the heart.
Subarachnoid Space (Actual space between the arachnoid mater and pia mater)
Vessels: Cerebral arteries and veins (e.g., arteries from the circle of Willis)
* The cerebral arteries (such as the anterior, middle, and posterior cerebral arteries) and veins run in the subarachnoid space, along with cerebrospinal fluid (CSF).
* A rupture of an aneurysm (e.g., a berry aneurysm) or trauma can lead to a subarachnoid hemorrhage (SAH), where blood fills the subarachnoid space, mixing with the CSF and causing irritation of the meninges (hence the thunderclap headache = meningeal irriation).
The intracerebal space (within the brain tissue itself)
Vessels: intracerebal vessels (the penetrating arteries and capillaries, and intracerebral veins)
The intracerebal arteries originate from the major cerebral arteries, which are located on the brain’s surface, in the subarachnoid space. They travel inward, passing through the pia mater (the innermost meningeal layer) and penetrating the brain tissue. The cappilaries tehy give rise to do not make contact with the meninges.
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Key understanding - the layers of the blood brain barrier are not the meninges but are much smaller cellular surrounding the deeper vessels - endothelial cells, basement memebrane, Pericytes, astrocyte end feets and microglial immune cells. The endothelial cells that form the BBB are located within the capillaries and small arteries inside the brain parenchyma, beneath the pia mater and the subarachnoid space. These cells have tight junctions that prevent certain substances from passing freely into the brain tissue.The BBB is not directly part of the meninges but is closely associated with the vessels that pass through or are surrounded by the pia mater. The subarachnoid space contains the major cerebral arteries and veins that supply and drain blood from the brain. As these vessels penetrate into the brain tissue, they are lined with endothelial cells that are part of the BBB.
Basically the BBB is not the meniges but is cellular wrapping around the vessels both when they penetrate and more superficially when they are in the meninges.
Intracranial Haemorrhage:
- What are the four types?
- What vessels are found in each space?
- Whate causes the vessles to rupture?
- appaerance on CT head?
- Typical clinical presentation for each
- Which types of intracranial (within the skull) haemorrhages are classed as haemorrhagic strokes?
Intracranial haemorrhage refers to bleeding within the skull. There are four types.
Extradural haemorrhage (bleeding between the skull and dura mater)
usually caused by a rupture of the middle meningeal artery in the temporoparietal region. It can be associated with a fracture of the temporal bone. mnemonic - mixed martial arts causes fractures.
On a CT scan, they have a bi-convex shape and are limited by the cranial sutures (they do not cross the sutures, which are the points where the skull bones join together because the dura is fused to the skull at these points). LEMONS
A typical history is a young patient with a traumatic head injury and an ongoing headache. They have a period of improved neurological symptoms and consciousness, followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents.
Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
Caused by a rupture of the bridging veins in the outermost meningeal layer
On a CT scan, they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures - because its below the dura, the dura connects to the sutures). BANANAS
Subdural haemorrhages may occur in elderly and alcoholic patients, who have more atrophy in their brains, making the vessels more prone to rupture. They typically develop more gradually (vein not an artery) following minor trauma (e.g. a fall).
Sx - Acute SDH usually present with reduced conciousness, chornic presents in elderly patients with with insideous onset headache, speech distrubance, N+V, weakness, personality changes.
Subarachnoid haemorrhage (bleeding in the subarachnoid space)
Bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.
CT appearence - hyperdense (bright) areas along the sulci (grooves on the brain surface) and around the cerebral cortex. It can also be seen in the ventricular system if it spreads there.
The typical history is a sudden-onset occipital headache during strenuous activity, such as heavy lifting or sex. The sudden and severe onset leads to the “thunderclap headache” description.
Stroke - sudden onset headache (neruological symptom)
Intracerebral haemorrhage (bleeding into brain tissue)
- ME: Rupture of the intracranial vells - perforation arteries, capillaries or intracranial veins
- occours spontaneously or secondary to ischemaic stroke, tumours o aneurism rupture
- CT appaerance - hyperdense within the brain parenchyma (looks like a white circle in a part of the brain - similar to a tumour).
It presents similarly to an ischaemic stroke with** sudden-onset focal neurological symptoms, such as limb or facial weakness, dysphasia or vision loss - it is a stroke**
stroke - sudden onset weakness, dysphagia or vision change (neurological symptom)
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THE TWO INTRACRANIAL BLEEDS THAT ARE CLASSIFIED AS STROKES:
Intracerebral (within the brain tissue) and Subarachnoid haemorrhages.
Remeber a stroke is any sudden onset (immediate to maximum intensity) neurological symptom.
2 Ix and 4 management of extra-/sub-dural haemorrhage?
- Ix - CT head and coagulation screen
- intubation and ventilation if conciousness is reduced
- correct any clotting abnormality
- correct any hypertension (big risk factor, alongside aneurism) - THIS IS KEY
Smaller bleeds may be managed conservatively with close monitoring and repeat imaging.
Surgical options for treating an extradural or subdural haematoma are:
Craniotomy (open surgery by removing a section of the skull) - expecially for the bottom two, and needed for aneurism repair)
Burr holes (small holes drilled in the skull to drain the blood) - extradural and subdurals, if small enough.
Subarachnoid can management is seperate but also involves aneurism repair using endovascular coiling or neurosurgical clipping. There is more detail and different medical management - nimodipine for preventing vasospasm.
The Glasgow Coma Scale (GCS) is a universal assessment tool for the level of consciousness.
- write out all 15 steps
- what is the most important factor progonstically?
- what are lateralising signs?
It is scored based on best eye opening response, best verbal response and best motor response
Mr Carroll - dont learn the numbers learn the stages for each.
The most important prognostically is motor, if nothing else learn this. Flexing to pain or better indicates a potential to recover, extending to pain or worse indicates a poor prognosis and is such that the patient may not be accepted by a neurosurgeon for treatment.
Best Motor Response
6. Obeys commands (raise you arms above your head)
5. Localises to pain (bats hands away)
4. Flexes to pain (reachs up to face but not all the way)
(3. Spastic flexion/’withdrawal’) AVOID USING THIS HEADING - harder to rememebr
2. Extends to pain - (straightens arms out in repsosne to pain)
1. None
LEARN THIS ^^^
Best Verbal Response
5. Orientated in time, place, and person
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
1. None
Best Eye Opening Response
4. Eyes open spontaneously
3. Eyes open to speech
2. Eyes open to pain
1. None
The best site for applying a pain stimulus is a point immediately below the ear between mastoid process posteriorly and mandible anteriorly, applying the stimulus bilaterally, equally, and ultimately as hard as one can.
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Lateralizing signs are neurological symptoms that suggest dysfunction in a particular hemisphere of the brain, and they are critical for localizing lesions or damage. They include motor deficits (hemiparesis/hemiplegia), gaze deviations, pupillary changes, speech or sensory impairments, focal seizures, and visual field defects, among others.
KEY
- What are the two types of Cerebrovascular accidents
- 3 Causes of Ischemia? KEY
- Definition of a TIA
- KEY - presentation of a stroke?
within 1/2 hours. A stroke is a cerebrovascular event that is caused by abnormal perfusion of cerebral tissue. Cerebrovascular accidents are either:
- Ischaemia or infarction of the brain tissue secondary to a disrupted blood supply (ischaemic stroke)
- Intracranial haemorrhage, with bleeding in or around the brain (haemorrhagic stroke)
A sudden onset of any neurological symptoms suggests a vascular cause (e.g., stroke). Stroke symptoms are typically asymmetrical.
Ischemic Stroke Causes:
- Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell).
- Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease.
- Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.
Transient ischaemic attack (TIA) involves temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction. Symptoms have a rapid onset and often resolve before the patient is seen. TIAs may precede a stroke. Crescendo TIAs are two or more TIAs within a week and indicate a high risk of stroke.
Common symptoms are sudden-onset, typically asymetrical:
Limb weakness
Facial weakness
Dysphasia (speech disturbance)
Visual field defects
Sensory loss
Ataxia and vertigo (posterior circulation infarction)
FAST mnemonic - sudden onset (fast) fascial weakness, arm (limb) weakness, dysphasia (speech disturnace). But also remember the other three
What is the anterioir and the posterior circulation and which vessels make up each?
What do the three cerebral arteries each supply?
The network of blood vessels that supply the brain are joined by the circle of Willis.
Many blood vessels supply different areas of the brain. These are broadly divided into the anterior and posterior circulation.
Anterior circulation: a network of blood vessels arising from the carotid arteries.
Posterior circulation: a network of blood vessels arising from the vertebrobasilar arteries.
Carotid system: the common carotid artery gives off the internal and external carotid arteries. The internal carotid artery is vital to the circle of Willis. It gives off the anterior and middle cerebral arteries as well as the posterior communicating artery.
Vertebrobasilar system: the two vertebral arteries join to form the basilar artery. Multiple branches arise from this artery. The basilar artery gives off the posterior cerebral arteries and joins anterior circulation via the posterior communicating artery.
Individual blood vessels correspond to areas of the brain that have specific motor, sensory, and/or high cortical functioning (e.g. speech).
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Cerebral arteries
There are three major cerebral vessels, which are connected by communicating arteries at the circle of Willis.
Anterior cerebral artery: supplies part of the frontal and parietal lobe. Part of the anterior circulation of the brain
Middle cerebral artery: supplies a large proportion of the lateral surface of each brain hemisphere including the internal capsule and basal ganglia. Most common site of infarction. Forms part of the anterior circulation of the brain
Posterior cerebral artery: supplies the occipital lobe and inferior proportion of the temporal lobe as well as some deep structures (e.g. thalamus). Forms part of the posterior circulation of the brain
Occlusion of these arteries leads to a characteristic set of clinical features corresponding to the motor and/or sensory functions they help control.
A stroke presents with sudden, focal neurological deficit that reflects the area of brain devoid of blood flow.
How do anterior and posteroir infarctions each present?
Brainstem syndromes are tested on the next card
Anterior ischaemic stroke:
Patients with anterior ischaemic strokes (i.e. TACS, PACS, LACS) develop a constellation of features dependent on the extent and location of the infarct.
1.Unilateral weakness and/or sensory deficit: face and/or arms and/or legs
2.Homonymous hemianopia: visual field loss on the same side of both eyes (make sense when you look up the tracts)
3.Higher cerebral dysfunction: dysphasia (language), visuospatial dysfunction (e.g. neglect, agnosia (recogniton))
Classically, an isolated infarction of the anterior cerebral artery leads to contralateral leg weakness only.
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Posterior ischaemic stroke
The posterior circulation is composed of the vertebrobasilar arterial system. This supplies the brainstem, cerebellum and occipital cortex. Therefore, posterior strokes can affect balance, vision, and cranial nerves. POCS account for 20-25% of ischaemic strokes
Dizziness
Diplopia
Dysarthria & Dysphagia
Ataxia
Visual Field defects
Brainstem syndromes: for example basilar artery leads to locked in syndrome, Posteroir inferioir cerebellar (not PCA) occlusion affects the medulla - Nystagmus, vertigo, diplopia, horners sydnrome, facial sensory loss, dysarthria
Brainstem/Posterioir storke syndromes
What is Wallenberg sybdrome?
What is locked in syndrome?
Posterior stroke syndromes
A collection of syndromes that occur due to infarction of specific posterior circulation arteries.
Commonly referred to as ‘brainstem syndromes’. Classical examples include ‘Wallenberg syndrome’ (posterior inferior cerebellar artery occlusion) or ‘locked-in syndrome’ (basilar artery occlusion).
Wallenberg syndrome, also known as lateral medullary syndrome due to its location, presents with a constellation of features:
Nystagmus
Vertigo
Ipsilateral Horner’s syndrome
Ipsilateral facial sensory loss
Dysarthria & dysphagia
Diplopia
Contralateral pain and temperature loss
Locked in syndrome (basaliar artery occlusion):
- Patients are aware and can think, but are unable to speak or move.
- complete paralysis apart from eye movemen - classically they can move their eyes vertically and blink but no more
THIS WAS TESTED!!
Ix and 2 steps to intial management for suspeted TIA? (resolved symptoms) 3 key things
Ix and initial management for suspected stroke?
Inital managemnet of a suspected stroke and a susepted TIA are different!!!
TIA:
TIA is a clinical diagnosis based on the history as the majority of patients will have complete resolution of symptoms. Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit
- The principle management for TIA is 300 mg of aspirin that is usually continued for two weeks , (clopidogrel will be added two week later as part of secondary prevention)
- Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode) - for bloods ECG and US carotid/CT angiogram.
- Diffusion-weighted MRI scan is the imaging investigation of choice - this isnt immediate, the daignosis is clinical
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Management of Stroke - GOT THIS WRONG!!!
Initial management involves:
- Exclude hypoglycaemia
- Immediate CT brain to exclude haemorrhage - Key Ix differs to TIA
- First line - Thrombolysis (w/ Alteplase - tissue plasminogen activator) if within 4.5 hours of symptom onset. Risk of Haemoeehage (monitoring), after the timeframe risk of haemorrage outweighs benefits…
- If thromboylsis is not appropriate, patients should be started immediately on 300 mg of aspirin for two weeks (then changed to clopidogrel) . If thrombolysis was given, aspirin is usually started 24-48 hours following treatment.
- Thrombectomy - CAN BE combineded with thrombolysis so thromboylsis is given immediately if possible… Thrombectomy is considered in patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation. It may be considered within 24 hours of the symptom onset and alongside IV thrombolysis.
In patients with an ischaemic stroke, lowering the blood pressure can worsen the ischaemia. High blood pressure treatment is only indicated in hypertensive emergency or to reduce the risks when giving intravenous thrombolysis. Blood pressure is aggressively treated in patients with a haemorrhagic stroke.
6 Neurological Deficits in a TIA (Harder)
A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.
Neurological deficits:
- Unilateral weakness or sensory loss
- Dysphasia
- Ataxia, vertigo, or incoordination
- Amaurosis fugax: transient monocular blindness
- Homonymous hemianopia: visual field loss on the same side of both eyes
- Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits
Amaurosis fugax:
This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.
The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.
Can patients drive after a stroke or TIA?
Cars and motorcycles: stop driving one month, do not need to inform DVLA
Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
After the inital management (MRI for TIA or CT for stroke), how are patients with a stroke or TIA are investigated for an underlying cause, 2 key things?
How are each of these causes managed?
Secondary prevention of stroke and TIA (the same)? - 4 things
Patients with a TIA or stroke are investigated for carotid artery stenosis and atrial fibrillation with:
Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
ECG or ambulatory ECG monitoring
Anticoagulation is initiated for atrial fibrillation (after excluding haemorrhage and finishing two weeks of aspirin).
Surgical interventions are considered where there is significant carotid artery stenosis. The options are:
Carotid endarterectomy (recommended in the NICE guidelines)
Angioplasty and stenting
TOM TIP: The top risk factors to remember are atrial fibrillation and carotid artery stenosis. All patients with a TIA or stroke will have carotid imaging and ECGs to identify these.
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Secondary Prevention
Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
Blood pressure and diabetes control
Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
Aspirin is aleady initiated in the immediate management and i think continues
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*Not testing myself but just be aware
*
Stroke patients require a period of adjustment and rehabilitation involving a multi-disciplinary team of:
Stroke physicians
Nurses
Speech and language (SALT) to assess swallowing
Dieticians in those at risk of malnutrition
Physiotherapy
Occupational therapy
Social services
Optometry and ophthalmology
Psychology
Orthotics
Atrial fibrillation:
Uncontrolled and unorganised activity in the atria leads to blood stagnating in the left atrium, particularly in the left atrial appendage. Eventually, this stagnated blood leads to a thrombus (clot). This thrombus then mobilises (becomes an embolus) and travels from the left atrium to the left ventricle, into the aorta and up in the carotid arteries to the brain. It can then lodge in a cerebral artery and cause an ischaemic stroke.
Without anticoagulation, patients with atrial fibrillation have around a 5% risk of stroke each year, depending on individual factors.With anticoagulation, patients with atrial fibrillation have around a 1-2% risk of stroke each year, depending on individual factors. Anticoagulation treatment carries around a 2.5-8% risk of serious bleeding each year, depending on individual factors.
QUESTION:
What two scores are used to calculate clot vs haemorrhage risk in patients with atrial fibrillation? Name the parts to each score and interpret the overall results…
Extra point - What is the immediate management for head injuries for patients that are on anti-coagulation?
CHA2DS2-VASc
CHA2DS2-VASc is a tool for assessing whether a patient with atrial fibrillation should start anticoagulation. It is a list of risk factors that increase the likelihood of a stroke. The higher the score, the higher the risk of developing a stroke or TIA.
CHA2DS2-VASc is a mnemonic for the factors that score a point:
C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)
NICE (2021) recommends, based on the CHA2DS2-VASc score:
0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation
Bleeding Risk
The NICE guidelines recommend using the ORBIT score for assessing the risk of major bleeding in patients with atrial fibrillation taking anticoagulation. The easiest way to calculate the ORBIT score is using an online calculator. The “ORBIT” mnemonic can be used to remember the 5 factors:
O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication
For most patients with atrial fibrillation, the risk of stroke with no anticoagulation will outweigh the risk of bleeding on anticoagulation.
The NICE guidelines (2021) recommend for anticoagulation:
Direct-acting oral anticoagulants (DOACs) first-line
Warfarin second-line, if DOACs are contraindicated
TOM TIP: Every patient with a head injury whilst taking anticoagulation should have a CT head to assess for an intracranial bleed, according to the NICE guidelines on head injuries (updated 2019). Being asked to review a patient after a fall is very common, and it helps to remember that a head injury plus anticoagulation automatically qualifies them for a CT scan. Inform patients starting on anticoagulation that they will need medical attention (A&E) in the event of a head injury for this reason.
Ataxia vs Dyskinesia
THIS IS FROM CHAT GTP
Ataxia
Definition: Ataxia is a lack of coordination and control over voluntary movements, usually caused by damage to the cerebellum, the part of the brain responsible for motor coordination and balance.
Characteristics: * Unsteady Gait: Difficulty walking and maintaining balance (ataxic gait). * Poor Coordination: Difficulty performing fine motor tasks like buttoning clothes or writing. * Impaired Speech: Slurred or slow speech (dysarthria). * Inconsistent Movements: Movements can be jerky and poorly coordinated, leading to tremors during voluntary actions. * Eye Movement Problems: Difficulty controlling eye movements (nystagmus). * Causes: Cerebellar damage (stroke, tumors, trauma), hereditary conditions (Friedreich’s ataxia, spinocerebellar ataxia), toxins, alcohol abuse, vitamin deficiencies. * Main Issue: Lack of coordination in movement.
Dyskineasia
Definition: Dyskinesia refers to involuntary, abnormal movements that occur due to dysfunction in the basal ganglia
Types of Invoultary Movements: * Chorea: Rapid, unpredictable, dance-like movements. * Athetosis: Slow, writhing movements. * Tremors: Rhythmic, shaking movements, typically seen in conditions like Parkinson’s disease. * Commonly Seen in Parkinson’s Disease: Dyskinesia often results from long-term use of medications like levodopa used to treat Parkinson’s disease. It can appear as writhing or jerking movements. * Tardive Dyskinesia: Involuntary movements, especially in the face or jaw, resulting from prolonged use of certain antipsychotic medications. * Causes: Medications (e.g., levodopa, antipsychotics), Parkinson’s disease, Huntington’s disease, brain injuries, and other conditions affecting the basal ganglia. * Main Issue: Involuntary movements that are excessive or erratic.
Your Supervisor said there are 4 key neurological emergencies
- Stroke
- Sudden onset headache
- seisure
- rapidly accending weakness
Types of Seizures seen in adults (5) and children (3)
Give a description of each seizsure type
The types generally seen in adults include:
Generalised tonic-clonic seizures
Partial seizures (or focal seizures)
Myoclonic seizures
Tonic seizures
Atonic seizures
The types more common in children include:
Absence seizures
Infantile spasms
Febrile convulsions
Generalised tonic-clonic seizures involve tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness. Typically, the tonic phase comes before the clonic phase. They are also called grand mal seizures. Before the seizure, patients might experience aura, an abnormal sensation that gives a warning that a seizure will occur. There may be tongue biting, incontinence, groaning and irregular breathing. After the seizure, there is a prolonged post-ictal period, where the person is confused, tired, and irritable or low.
Partial seizures (or focal seizures) occur in an isolated brain area, often in the temporal lobes. They affect hearing, speech, memory and emotions. Patients remain awake during partial seizures. They remain aware during simple partial seizures but lose awareness during complex partial seizures. There are various symptoms associated with partial seizures, depending on the location of the abnormal electrical activity:
Déjà vu
Strange smells, tastes, sight or sound sensations
Unusual emotions
Abnormal behaviours
Myoclonic seizures present with sudden, brief muscle contractions, like an abrupt jump or jolt. They remain awake. Myoclonic seizures can occur as part of juvenile myoclonic epilepsy in children.
Tonic seizures involve a sudden onset of increased muscle tone, where the entire body stiffens. This results in a fall if the patient is standing, usually backwards. They last only a few seconds, or at most a few minutes.
Atonic seizures (causing “drop attacks”) involve a sudden loss of muscle tone, often resulting in a fall. They last only briefly, and patients are usually aware during the episodes. They often begin in childhood. They may be indicative of Lennox-Gastaut syndrome.
Absence seizures are usually seen in children. The patient becomes blank, stares into space, and then abruptly returns to normal. During the episode, they are unaware of their surroundings and do not respond. These typically last 10 to 20 seconds. Most patients stop having absence seizures as they get older.
Infantile spasms are also known as West syndrome. It is a rare (1 in 4,000) disorder starting at around six months of age. It presents with clusters of full-body spasms. Hypsarrhythmia is the characteristic EEG finding. It is associated with developmental regression and has a poor prognosis. Treatment is with ACTH and vigabatrin.
Febrile convulsions are tonic-clonic seizures that occur in children during a high fever. They are not caused by epilepsy or other pathology (e.g., meningitis or tumours). Febrile convulsions occur in children aged between 6 months and 5 years. Febrile convulsions do not usually cause any lasting damage. One in three will have another febrile convulsion. They slightly increase the risk of developing epilepsy.
Initial investigations for seizure? 4
Specilist investigations for epilepsy? 2
Long-term Management?
Sepcialist Investigations for susepcted epilepsy:
- EEG: An electroencephalogram (EEG) shows typical patterns in different forms of epilepsy and supports the diagnosis.
- MRI brain is used to diagnose structural pathology (e.g., tumours).
Initial investigations to consider with seizsure exclude associated pathology (other than epilepsy):
- ECG - cardiac syncope
- Serum electrolytes, including sodium, potassium, calcium and magnesium
- Blood glucose - rule out hypoglycaemia and diabetes
- Blood cultures, urine cultures and lumbar puncture where sepsis, encephalitis or meningitis is suspected
Management
- inform the DVLA until seizure free for a year
- Women - Lamotrigine or Levetiracetam for all seizure types, except ethosuximate used for absent seizsures
- Zero to finals still says men - sodium valproate first line for generalise and tonic seizsures, However, i think this is outdated because of the sodium valproate pregnancy prevention programme…
What are the side effects of sodium valproate - name 3
Who can it not be prescribed to?
Sodium valproate works by increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brain. Notable side effects include:
**Teratogenic (harmful in pregnancy) - causes neural tube defects and developmental delay
**Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility
The new restrictions mean no one under the age of 55 will be newly prescribed sodium valproate unless two specialists agree there is no other effective or tolerated treatment, or unless there are “compelling reasons that the reproductive risks do not apply”. It used to apply to women who had to be on a form of contraception and sign a form acknowledging the risks of valproate.
Define Status Epilepticus?
What is the management of status?
- First, Second and Third line
- 3 formulations for first line?
Status epilepticus is a medical emergency defined as either:
A seizure lasting more than 5 minutes
Multiple seizures without regaining consciousness in the interim
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It is managed with an ABCDE approach invovling securing the airway, giving oxygen and ensuring IV access, and checking BMs
Medical treatment involves:
A benzodiazepine first-line, repeated after 5-10 minutes if the seizure continues
Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
Third-line options are phenobarbital or general anaesthesia
Options for benzodiazepines are:
Buccal midazolam (10mg) - M for mouth
Rectal diazepam (10mg) - D for derrier
Intravenous lorazepam (4mg) - l looks like an I for IV
Presentation of Syncope vs Seizure
Syncope vs seizure
Prolonged upright position before the event, lightheadedness, clammy, blurred vision before event
VS Epilepsy aura - smells, tastes, deja vu before the event
Reduced tone during the episode (although there may be some convulsion activity in syncope)
VS Tonic clonic activity, abnormal limb movmeent, head turning and may have tongue biting
Return of consciousness shortly after falling - seconds to a minute as blood flow returns to the brain
VS lasts more than five minutes
No prolonged post-ictal period - they may feel a bit groggy
VS postictal seizures patients have prolonged confusion, drowsiness, irritability and disorientation
There may be incontinence with both seizures and syncopal episodes.
Pathophysiology of parkinsons
Classic Triad of Parkinsonism
Sx of Parkinson’s - key features and 4 non-motor symptoms
Parkinson’s disease is a condition where there is a progressive reduction in dopamine in the basal ganglia, leading to disorders of movement. The symptoms are characteristically asymmetrical, with one side of the body affected more. The typical patient is an older man, around 70 years old, with a gradual onset of symptoms.
There is a classic triad of features in Parkinson’s disease:
Resting tremor (a tremor that is worse at rest)
Rigidity (resisting passive movement - muscle resist stretch/tight)
Bradykinesia (slowness of movement)
How to remeber it is resting tremor - the basal ganglia are all about controlling voluntary movements and when their function is affected you get involuntary movements (disinhibition). They are also responsible for co-ordinating habitual movements like walking, which slow down as their function is lost.
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Features:
- Resting “pill-rolling” tremor - improves with movement
- Cogwheel rigity - tremor on top of rigidity
- Bradykinesia (slower, smaller movements/fatiguing with use) presents as:
- hypomimia (reduced facial expression)
- Gait: loss of arm swing is an early sign, shuffling gait, difficulty initiating movement and turning around
- micrographia (smaller handwriting)
- reduced armswing
- reduced amplitude with repetative movements
Also presents with other non-motor features:
- sleep disturbance and insomnia
- cognitive impairement and memory problems
- postural instability (Risk of falls)
- anosmia - loss of sense of smell
- LUTs symptoms, incontinence and sexual dysfunction
Parkinson’s Tremor vs Benign Essential tremor
Parkinson’s
- Asymetrical
- worse at rest
- Other parkinson’s features
- worse with alcohol
- slower 4-6Hz
Benign Essential tremor:
- symmetrical (although not always i think)
- worse with movement (cant drink from a cup)
- isolated tremor
- improves with alcohol - Jane loves a drink
- Faster 6-12Hz, also commonly not just hands (Jane’s voice and head move)
Parkinson’s Disease:
- How is diagnosis made
Management:
- 4 treatment options
- synthetic dopamine is always combined with?
- an example of each
- basic mechanism of action for each?
- Side effect of Levodopa, Rx?
Clinical diagnosis based on signs (examination) and symptoms (history)
DaT (Dopamine Transmission) scan shows loss of doperminergic neurones in the basal ganaglia when there is doubt surroudning the diagnosis. (Comma shaped (normal) -> full stop with (loss in parkinsons)
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Management:
No treatment slows progression, they are about symptomatic control. Patients may describe themselves as “on” when the medications are acting, and they are moving freely, and “off” when the medications wear out, they are experiencing symptoms and their next dose is due.
The treatment options are:
Levodopa (combined with peripheral decarboxylase inhibitors, which stop it being metabolised in the body before reaching the brain)
COMT inhibitors
Dopamine agonists
Monoamine oxidase-B inhibitors
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Synthetic Dopamine - Levodopa: Co-beneldopa (levodopa and benserazide)
Side effect is dyskinesia (excessive motor activity):
- dystonia (abnormal movements)
- chorea (involvuntary moevements)
- athetosis (involuntary twisting or writhing movements)
Rx with amantadine (glutamate antagonist)
This is the most effective treatment so saved until it is needed
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COMT Inhibitors - Entacapone (C-apone for Comt)
COMT metaolises levodopa in the body (mainly) and the brian. It can be needs to be taken with Levodopa and it extends its half life.
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Dopamine Agonists - Bromocryptine
stimulate dopamine receptors but are different structure to dopamine - less effective
Me - Dopamine inhibitors pituitary - bromocryptine used in hyperporlactinaemia -
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MOA-B inhibitors- Selegiline (selective for dopamine breakdown)
mononamine (dopamine) oxidase (breakdown) inhibitors - inhibitors dopamine breakdown in the brain. Selective for dopamine over other monoamines like glutamate, seritonin….
What are Parkinson’s plus syndromes?
Key additional features 3/4
Parkinson’s plus syndromes are conditions that have the same classical triad of parkinson’s symptoms but with further symptoms:
Multiple Systems atrophy - multiple areas of the brain degenerate, including the basal ganglia (hence parkinsonism) but also there is widespread autonomic dysfunction (postural hypotension, abnormal sweating and sexual dysfuntion)
Demmentia with Lewy bodies - Parkinsonism with progressive conitive declcine,visual hallucinations , delusions, REM sleep disorders
Progressive supranuclear palsy - in the name affects eye movement (supranuclear area in the brainstem control eye movement)
Corticobasal degeneration…
What is benign essential tremor?
Features?
Management? -2
Benign essential tremor is a relatively common condition associated with older age. It is characterised by a fine tremor affecting all the voluntary muscles. It affects voluntary movements - It is most notable in the hands but can affect other areas, for example, causing a head tremor, jaw tremor and vocal tremor.
Features
Fine tremor (6-12 Hz)
Symmetrical
**More prominent with voluntary movement - this is key, Jane can’t hold a cup
**Worse when tired, stressed or after caffeine
Improved by alcohol - Jane drinks because of her tremor
Absent during sleep
Diagnosis is clinical.
Rx:
There is no definitive treatment for benign essential tremor. Medications that may improve symptoms are:
Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)
What is the mechanism behind drug induced parkinsonism?
What drugs cause it?
Drug-Induced Parkinsonism: A form of secondary parkinsonism caused by medications that block dopamine receptors or deplete dopamine.
Key Features:
- Resting tremor, rigidity, bradykinesia, and postural instability (similar to Parkinson’s disease).
- Often symmetrical (unlike idiopathic Parkinson’s).
- No progression after stopping the causative drug.
Common Causes:
- Antipsychotics (e.g., haloperidol, risperidone).
- Antiemetics (e.g., prochlorperazine (BPPV), metoclopramide).
- Calcium channel blockers (e.g., flunarizine, cinnarizine).
Myasthenia Gravis:
- what is myasthenia gravis?
- associated condition
- pathophysiology
- presentation?
Myasthenia means affecting the Neuromuscular juntion. Myasthenia gravis is an autoimmune condition affecting the neuromuscular junction that gets progressively worse with activity and improves with rest.
Myasthenia gravis affects men and women at different ages, typically affecting women under 40 and men over 60.
There is a strong link with thymomas (thymus gland tumours). 10-20% of patients with myasthenia gravis have a thymoma. 30% of patients with a thymoma develop myasthenia gravis.
Pathophysiology:
- Acetylcholine receptor Antibodies bind to the post synaptic acetyl chiline receptors, blocking them from recieving stimulation from Ach. The more the receptors are used in muscle contraction, the more they become blocked causing progressive weakness with activity.
Presentation:
Can be mild or life-threaningly severe. Most commonly affects the proximal muscles of the limsb and the small muscles of the head and neck :
- Difficulty climbing stairs, standing from a seat or raising their hands above their head
- Extraocular muscle weakness, causing double vision (diplopia)
- Eyelid weakness, causing drooping of the eyelids (ptosis)
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in the jaw when chewing
- Slurred speech
On examination - repeated blinking exercerbates ptosis, prolongued upward gazing exercerbated diplopia, and repated arm abduction will result in weakness
Different from Guillaine Barre - ascending parlytic polyneuropathy - emergency with rapidly accending weakness, starting in the legs, caused by molecular mimicry from campy antibodies (after gastro) attacking motor neurones/myeline sheath. Myasthenia gravis is a chronic condition. Just putting this in because you used to get confused but i think startin to clear this up now.
Myathenia Gravis Cont…
- Ix - 3?
- Treatment options?
- What is a myathenic crisis and how is it managed?
Ix:
Antibody tests look for:
AChR antibodies (around 85%) - just be aware of the others…
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)
CT or MRI of the thymus gland to look for thymoma
Endophonium test only where there is doubt - neostigmine (AchEstare inhibitor relieves the weakness) becuase it induces bradycardia. Positive result - causes improvement in Sx.
NOT CONDUCTION STUDIES - THAT IS GUILLAIN BARRE, demylination, in myathenia the nerve conduction is fine, its the NMJ!!!
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Treatment options:
Treatment options include:
First line - Pyridostigmine is a cholinesterase inhibitor that prolongs the action of acetylcholine and improves symptoms
Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies
Thymectomy can improve symptoms, even in patients without a thymoma
Rituximab (a monoclonal antibody against B cells) is considered where other treatments fail
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Myasthenic Crisis
Myasthenic crisis is a potentially life-threatening complication of myasthenia gravis. It causes an acute worsening of symptoms, often triggered by another illness, such as a respiratory tract infection. Respiratory muscle weakness can lead to respiratory failure. Patients may require non-invasive ventilation or mechanical ventilation.
Treatment is with IV immunoglobulins and plasmapheresis. - SAME AS GB
OMG THIS IS WHERE THE CONFUSION COMES FROM WITH HUILLAINE BARRER, A MYATHENIC CRISIS IS A BIT LIKE GUILLANE BARRE WHERE YOU GET RESPIRATORY INVOVLEMENT AND BOTH ARE MANAGED THE SAME WAY. BOTH ARE CAUSED BY ANTIBODIES BUT MYASTHENIA TO THE ACHR IN THE NMJ, GB TO THE MYELIN SHEATH AFFECTING NERVE CONDUCTION
remember can browse in deck to look at the presentation and patho
A brief summary on lambert-eaton myathenic syndrome:
- associated with?
- antibodies against?
- management?
Lambert-Eaton myasthenic syndrome is an autoimmune condition affecting the neuromuscular junction, similar to myasthenia gravis. The symptoms tend less pronounced than myasthenia gravis.In most cases, it is a paraneoplastic syndrome occurring alongside small-cell lung cancer (SCLC). It can also occur as a primary autoimmune disorder without the presence of SCLC.
Antibodies target and damage voltage-gated calcium channels in the presynaptic membrane of the neuromuscular junction, invovled in release of Ach across the synapse.
Symptoms are similar with proximal muscle weakness but, in contrast to with MG, symptoms improve with activity and are worse at rest.
Excluding underlying malignancy (e.g., small-cell lung cancer) is essential.
Amifampridine is the management (Ami = friend, Fam = family, Pre = pre-drinks, dine = dean of uni)
I wouldnt learn much more than this, too much to memorise but reacon could save your skin in an exam one day
