Neurology Flashcards
What is Stroke
a cerebrovascular accident
can either be
- Ischaemia (85%) or haemorrhage (15%)
What is Intracranial Haemorrhage
bleeding within the brain
What are 4 types of Intracranial haemorrhages
Extradural haemorrhage
Subdural haemorrhage
Intracerebral haemorrhage
Subarachnoid haemorrhage
what is a Intracerebral haemorrhage
bleeding into brain tissue
What is Subarachnoid haemorrhage
bleeding in the subarachnoid space from ruptured circle of willis
where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane
What is a Extradural haemorrhage
bleeding between the skull and dura mater
What is a Subdural haemorrhage
bleeding between the dura mater and arachnoid mater
What are RF for Intracranial Haemorrhage
Head injuries
Hypertension
Aneurysms
Ischaemic strokes (progressing to bleeding)
Brain tumours
Thrombocytopenia (low platelets)
Bleeding disorders (e.g., haemophilia)
Anticoagulants (e.g., DOACs or warfarin)
How do Intracerebral haemorrhag present
sudden-onset focal neurological symptoms, such as limb or facial weakness, dysphasia or vision loss.
What is most common cause of extradural haemorrhage
rupture of the middle meningeal artery in the temporoparietal region
fracture of temporal bone
How does Extradural haemorrhage present on CT
bi-convex shape and are limited by the cranial sutures
lemon shaped
what is typical presentation of Extradural haemorrhage
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
What is most common cause of subdural haemorrhage
rupture of the bridging veins in the outermost meningeal layer
How does subdural haemorrhage present on CT
a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).
moon shaped
what is typical presentation of subdural haemorrhage
elderly and alcoholic patients, who have more atrophy in their brains, making the vessels more prone to rupture.
or shaken baby
What is most common cause of Subarachnoid haemorrhage
ruptured cerebral aneurysm.
berry aneurysm ACA
what is typical presentation of Subarachnoid haemorrhage
sudden-onset occipital headache during strenuous activity
“thunderclap headache” description.
Neck stiffness
Photophobia
Vomiting
Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)
What is 1st line investigation for Subarachnoid haemorrhage
NCCT head
hyper-attenuation in the subarachnoid space
Star shaped
What is GS investigation for Subarachnoid haemorrhage and what will it show
Lumbar puncture
Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
Xanthochromia (a yellow colour to the CSF caused by bilirubin)
How is source of bleeding located in Subarachnoid haemorrhage
CT angiography
How are cerebral aneurysms surgically managed
endovascular coiling
neurosurgical clipping,
WHat is a complication of Subarachnoid haemorrhage and how is it managed
Vasospasm - brain ischaemia
Nimodipine is a calcium channel blocker
How are Intracranial Haemorrhages investigated
Immediate imaging (e.g., CT head) is required to establish the diagnosis.
Bloods should include a full blood count (for platelets) and a coagulation screen.
How are Intracranial Haemorrhage initially managed
- Admission to a specialist stroke centre
- Discuss with a specialist neurosurgical centre to consider surgical treatment
- Consider intubation, ventilation and intensive care if they have reduced consciousness
- Correct any clotting abnormality (e.g., platelet transfusions or vitamin K for warfarin)
- Correct severe hypertension but avoid hypotension
ABCDE
What are surgical options for treating an extradural or subdural haematoma
Craniotomy (open surgery by removing a section of the skull)
Burr holes (small holes drilled in the skull to drain the blood)
What GCS requires airway support
8/15
minimum score 3/15
How is Glasgow Coma Scale (GCS) scored
eyes, verbal response and motor response
motor /6
verbal /5
eyes /4
What is Ischaemia
inadequate blood supply
What is infarction
tissue death due to ischaemia
What can cause blood supply to brain to become disrupted
A thrombus or embolus
Atherosclerosis
Shock
Vasculitis
What is Transient ischaemic attack (TIA)
temporary neurological dysfunction caused by ischaemia but without infarction
What are symptoms of TIA
rapid onset and often resolve before the patient is seen
What are Crescendo TIAs
two or more TIAs within a week and indicate a high risk of stroke
How is TIA investigated
diffusion weighted MRI
what is the long term management of TIA
- first 21 days after attack = clopidogrel + Aspirin
- after 21 days = Clopidogrel
- if high lipids then + a high-intensity statin (atorvastatin)
what prophylaxis medication is given with aspirin
PPI
How is TIA managed initially
aspirin 300mg
review within 24 hours
How does stroke present
sudden onset of neurological symptoms suggests a vascular cause (e.g., stroke)
typically asymmetrical
- Limb weakness
- Facial weakness
- Dysphasia (speech disturbance)
- Visual field defects
- Sensory loss
- Ataxia and vertigo (posterior circulation infarction)
How strokes classified
Oxford Stroke Classification (Bamford)
What criteria is assessed in Bamford classification
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
What is Total anterior circulation infarcts (TACI, c. 15%)
3/3
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
What do Total anterior circulation infarcts involve
involves middle and anterior cerebral arteries
What is Partial anterior circulation infarcts (PACI, c. 25%)
and 2/3
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
What do Partial anterior circulation infarcts involve
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
What is Lacunar infarcts (LACI, c. 25%)
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis
subcortical stroke
what is Posterior circulation infarcts (POCI, c. 25%)
involves vertebrobasilar arteries
damage to cerebellum and brainstem.
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
What are associated effects of anterior cerebral artery stroke
- lower limb > upper affected and no face or speech impairment
What are associated effects of middle cerebral artery stroke
- upper >lower limb + speech impaired, contralateral homonymous hemianopia
What are associated effects of posterior cerebral artery stroke
- Contralateral homonymous hemianopia with macular sparing
- Visual agnosia
What are associated effects of Lateral medullary syndrome (PICA)
- ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
- contralateral: limb sensory loss
What are associated effects of Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain) stroke
- Ipsilateral CN III palsy
- Contralateral weakness of upper and lower extremity
what is CN III palsy
eye turns down and out
double vision
What are associated effects of Basilar artery stroke
‘Locked-in’ syndrome
What are Rf for ischaemic stroke
age
hypertension
smoking
hyperlipidaemia
diabetes mellitus
atrial fibrillation
What are Lacunar infarcts
small infarcts around the basal ganglia, internal capsule, thalamus and pons
What are Rf for Haemorrhagic stroke
age
hypertension
arteriovenous malformation
anticoagulation therapy
What increases the risk of stroke in patients on Combined contraceptive pill
migraines with aura, smokers over 34 years or those with a history of stroke or TIA.
What is FAST tool
used in community to ID stroke
F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)
What is ROSIER tool
(Recognition Of Stroke In the Emergency Room) gives a score based on the clinical features and duration.
Stroke is possible in patients scoring one or more.
what is CHA2D2VASC
the risk of stroke in AF patients.
- congestive heart failure
- hypertension
- age ≥75 (doubled)
- diabetes (doubled)
- vascular disease
- age 65 to 74
- sex category (female).
What is ORBIT
RF for bleeding
- older (75 years or older)
- reduced haemoglobin
- bleeding history
- insufficient kidney function (eGFR < 60 mg/dL/1.73 m2)
- treatment with an antiplatelet agent
What is ABCD2
used to determine the risk for stroke in the days following a transient ischemic attack
age
BP
clinical features
DM
Duration of Sx
What is the first line radiological investigation for suspected stroke
non-contrast CT head scan
How do acute ischaemic strokes present on CT
‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately
How do acute haemorrhagic strokes appear on CT
typically show areas of hyperdense material (blood) surrounded by low density (oedema)
What is the initial management of ischaemic stroke
Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
Admission to a specialist stroke centre
How is Ischaemic stroke treated if presenting within 4.5 24
Thrombolysis with alteplase
What is alteplase
tissue plasminogen activator
What should blood pressure be lowered to before thrombolysis
185/110 mmHg
How is Ischaemic stroke treated WITHIN 6hrs hours
Thrombectomy
if also under 4.5hr then IV thrombolysis
How is Ischaemic stroke treated WITHIN 24hrs hours
Thrombectomy
Where does a thrombus/embolus have to be located to use Thrombectomy
proximal anterior circulation or proximal posterior circulation
When is High blood pressure treatment indicated in stroke treatment
only in hypertensive emergency
with ischaemic stroke lowering the blood pressure can worsen the ischaemia
How are patients assessed for underlying causes in stroke
carotid artery stenosis and atrial fibrillation with:
Carotid imaging (e.g., carotid duplex ultrasound, or CT or MRI angiogram)
ECG or ambulatory ECG monitoring
How is Afib managed
Anticoagulation –> Apixaban
How is carotid artery stenosis managed
Carotid endarterectomy (if the stenosis > 50%)
Angioplasty and stenting
What is Secondary Prevention for stroke
- 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)
What people are involved in stroke rehabilitation MDT
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
how does pontine haemorrhage present
reduced GCS, paralysis and bilateral pin point pupils
What is dementia
progressive and irreversible impairment in memory, cognition, personality and communication
what is early onset dementia
when the symptoms start before aged 65.
what is Mild cognitive impairment
a deficit in cognition and memory that is greater than expected with age but not significant enough for a diagnosis of dementia
usually live independently
What is Alzheimers dementia
MC type of dementia
progressive degenerative disease of the brain
pathophysiology involves brain atrophy, amyloid plaques, reduced cholinergic activity and neuroinflammation
What is Vascular dementia
2nd MC type of dementia
vascular damage and impaired blood supply to the brain.
WHat are RF for vascular dementia
History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular
What is Dementia with Lewy bodies
alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
What are associated symptoms of Dementia with Lewy bodies
visual hallucinations, delusions, REM sleep disorders and fluctuating consciousness.
What are the macroscopic pathological changes associated with Alzheimers
widespread cerebral atrophy, particularly involving the cortex and hippocampus
What are the microscopic pathological changes associated with Alzheimers
- cortical plaques due to deposition of type A-Beta-amyloid protein
- intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
- hyperphosphorylation of the tau protein
What are the biochemical pathological changes associated with Alzheimers
deficit of acetylcholine from damage to an ascending forebrain projection
What happens to tau proteins in AD
Neurofibrillary tangles; filaments made from protein called tau
excessively phosphorylated, impairing its function
What are the main subtypes of VD
Stroke-related VD - multi-infarct or single-infarct dementia
Subcortical VD - caused by small vessel disease
Mixed dementia - the presence of both VD and Alzheimer’s disease
How do patients with vascular dementia present
Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.
What are symptoms of Vascular dementia
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
What could an MRI show for vascular dementia
infarcts and extensive white matter changes
How can Lewy body dementia be differentiated from Parkinsons
LBD = progressive cognitive impairment typically occurs before parkinsonism symptoms
PD = motor symptoms typically present at least one year before cognitive symptoms
What special investigation can be used for Lewy body dementia with high specificity
single-photon emission computed tomography (SPECT)
DaTscan.
What are 3 classic features of Parkinsons
Bradykinesia
Tremor (pill rolling)
Rigidity (lead pipe, cog wheel)
What medication should be avoided in Lewy body dementia
neuroleptics aka antipsyhotics as v sensitive and can cause irreversible parkinsonism
What type of medication can have cognitive impairment, memory impairment or personality changes.
Medications with an anticholinergic effect,
Name 3 types of medication with an anticholinergic effect
Anticholinergic urological drugs (e.g., oxybutynin, solifenacin and tolterodine)
Antihistamines (e.g., chlorphenamine and promethazine)
Tricyclic antidepressants (e.g., amitriptyline)
What are psychiatric DDx for dementia
Depression
Psychosis
Delirium (e.g., secondary to infection)
What are neurological DDx for dementia
Brain tumours (particularly affecting the frontal lobes)
Parkinson’s disease
Huntington’s disease
Progressive supranuclear palsy
What are endocrine DDx for dementia
Hypothyroidism
Adrenal insufficiency
Cushing’s syndrome
Hyperparathyroidism (causing hypercalcaemia)
What are nutritional DDx for dementia
Vitamin B12 deficiency
Thiamine deficiency (causing Wernicke-Korsakoff syndrome)
What are modifiable Risk Factors for dementia
Exercise
Mental stimulation (e.g., a more mentally challenging job)
Maintaining a healthy weight (obesity increases the risk)
Blood pressure control (hypertension increases the risk)
Blood glucose control (diabetes increase the risk)
What are early symptoms of dementia
Forgetting events
Forgetting names
Difficult remembering words
Repeatedly asking the same questions
Impaired decision making
Reduced flexibility
What are features of advanced dementia
- Inability to speak or understand speech (aphasia)
- Swallowing difficulties (dysphagia), which can lead to aspiration and pneumonia
- Appetite and weight loss
- Incontinence
what are memory screening testes that can be used at the initial presentation
Six Item Cognitive Impairment Test (6CIT)
10-point Cognitive Screener (10-CS)
Mini-Cog
General Practitioner Assessment of Cognition (GPCOG)
Montreal Cognition Assessment (MoCA)
What additional blood tests can be ordered to exclude dementia DDx
Full blood count
Urea and electrolytes
Liver function tests
Inflammatory markers (e.g., CRP and ESR)
Thyroid profile
Calcium
HbA1c
B12 and folate
What investigations can be ordered to exclude dementia DDx
Mid-stream urine (MSU) if infection is suspected
Chest x-ray (if lung cancer is suspected)
MRI brain) to exclude structural pathology.
What 5 domains are tested in Addenbrooke’s Cognitive Examination-II
Attention
Memory
Language
Visuospatial function
Verbal fluency
What score indicate possible dementia in Addenbrooke’s Cognitive Examination-II
88 or less
What plannung steps can be taken for patient with dementia
- Lasting power of attorney
- Advanced decisions
- Planning future care, including places and end-of-life care
What are medication options for Alzheimers
- Acetylcholinesterase inhibitors (e.g., donepezil, rivastigmine or galantamine)
- Memantine, which works by blocking N-methyl-D-aspartic acid (NMDA) receptors
Name 3 Acetylcholinesterase inhibitors
donepezil, rivastigmine or galantamine
What behavioural and psychological symptoms of dementia (BPSD) include
Depression
Anxiety
Agitation
Aggression
Disinhibition (e.g., sexually inappropriate behaviour)
Hallucinations
Delusions
Sleep disturbance
What initial steps can be taken to manage behavioural and psychological symptoms of dementia
Treating underlying causes (e.g., pain, constipation or urinary retention)
Environmental factors (e.g., providing a calming setting and removing triggers)
Appropriately trained carers
Appropriate supervision (one-to-one observation may be required)
Music therapy
What are common features of frontotemporal lobar dementias
initial presentation typically involves abnormalities in behaviour, speech and language
Relatively preserved memory
early onset 40-60
What medication can be taken to manage behavioural and psychological symptoms of dementia
SSRI antidepressants for depressive symptoms
Antipsychotic drugs (typically risperidone first-line)
Benzodiazepines (only for crisis management)
What factors favor delirium over dementia
- acute onset
- impairment of consciousness
- fluctuation of symptoms: worse at night, periods of normality
- abnormal perception (e.g. illusions and hallucinations)
- agitation, fear
- delusions
What can cause delirium
Constipation
Hypoxia
Infection
Metabolic disturbance
Pain
Sleeplessness
Prescriptions
Hypothermia/pyrexia
Organ dysfunction (hepatic or renal impairment)
Nutrition
Environmental changes
Drugs (over the counter, illicit, alcohol and smoking)
CHIMPS PHONED
What are features of hyperactive delirium
Agitation
Delusions
Hallucinations
Wandering
Aggression
What are features of hypoactive delirium
Lethargy
Slow
Sleepy
Inattention
What are investigations are included in a confusion screen
Blood tests:
FBC (e.g. infection, anaemia, malignancy)
U&Es (e.g. hyponatraemia, hypernatraemia)
LFTs (e.g. liver failure with secondary encephalopathy)
Coagulation/INR (e.g. intracranial bleeding)
TFTs (e.g. hypothyroidism)
Calcium (e.g. hypercalcaemia)
B12 + folate/haematinics (e.g. B12/folate deficiency)
Glucose (e.g. hypoglycaemia/hyperglycaemia)
Blood cultures (e.g. sepsis)
Urinalysis:
UTI
CT head: if there is concern about intracranial pathology (bleeding, ischaemic stroke, abscess)
Chest X-ray: may be performed if there is concern about lung pathology (e.g. pneumonia, pulmonary oedema)
clinical signs/investigations that suggest delirium
Vital signs (e.g. fever in infection, low SpO2 in pneumonia)
Level of consciousness (e.g. GCS/AVPU)
Evidence of head trauma
Sources of infection (e.g. suprapubic tenderness in urinary tract infection)
Asterixis (e.g. uraemia/encephalopathy)
WHat is 1st line medication option for delirium
Haloperidol (oral, IV or IM)
If benzodiazepines are to be used, lorazepam is first-line
What steps can be taken to prevent episodes of delirium
- Avoid drugs known to precipitate delirium (e.g. opiates and benzodiazepines)
- Identify patients at higher risk of developing delirium and observe them closely for early signs of delirium
- Assess other factors which may induce or exacerbate delirium (e.g. pain control, drugs etc)6
- Employ supportive/environmental management approaches for all patients, regardless of delirium risk
What are environmental adaptation management strategies to manage delirium
access to a clock and other orientation reminders
familiar objects where possible
Involve the family, friends and/or carers
control the level of noise, temperature and light
What are general supportive adaptation management strategies to manage delirium
consistent nursing and medical team
patient has access to aids
Enable the patient to do what they can for themselves
What is Parkinson’s disease
progressive reduction in dopamine in the substantia nigra pars compacta, leading to disorders of movement
Are parkinsons symptoms symmetrical or asymmetrical
asymmetrical
What is the parkinsons triad
Resting tremor (a tremor that is worse at rest)
Rigidity (resisting passive movement)
Bradykinesia (slowness of movement)
What does someone with parkinsons look like when walking
maks like face
stooped posture
forward tilt
reduced arm swinging
shuffling gair
What is the basal ganglia responsible for
coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patterns.
What are features of a Parkinson’s Tremor
Asymmetrical
4-6 hertz (cycles 4-6 times a second
Worse at rest
Improves with intentional movement
No change with alcohol
How can Bradykinesia present in Parkinsons
Handwriting gets smaller and smaller (micrographia)
Small steps when walking (“shuffling” gait)
Rapid frequency of steps to compensate for the small steps and avoid falling (“festinating” gait)
Difficulty initiating movement (e.g., going from standing still to walking)
Difficulty in turning around when standing and having to take lots of little steps to turn
Reduced facial movements and facial expressions (hypomimia)
What are other features of Parkinsons
Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Postural instability (increasing the risk of falls)
Cognitive impairment and memory problems
What is “cogwheel” rigidity describe
jerking resistance to movement
What are features of a Benign Essential Tremor
Symmetrical
6-12 hertz
Improves at rest
Worse with intentional movement
No other Parkinson’s features
Improves with alcohol
What are DDx of a tremor
Parkinson’s disease
Multiple sclerosis
Huntington’s chorea
Hyperthyroidism
Fever
Dopamine antagonists (e.g., antipsychotics)
What medication can improve symptom of benign essential tremor
Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)
What are Parkinson’s-Plus Syndromes
Multiple system atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration
What is Multiple System Atrophy
Parkinsonism with associated autonomic disturbance (atonic bladder, postural hypotension)
How is Parkinson’s disease diagnosed
diagnosed clinically based on the history and examination findings
UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.
What is the diagnostic criteria from UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria Diagnosis of a Parkinsonian syndrome
presence of bradykinesia
plus at least one of the following:
- Muscular rigidity
- Resting tremor (4-6 Hz frequency)
- Postural instability (not caused by a visual, vestibular, cerebellar or proprioceptive dysfunction)
In addition to Parkinsonian syndrome criteria what also must be included for Parkinsons diagnosis
- Exclusion criteria –> Hx of stroke, encephalitis, head injury…
- Supportive positive criteria –> response to med, unilateral onset, progressive disease…
What is the diagnostic criteria from the ‘International Parkinson and Movement Disorder Society’ for diagnosis of benign essential tremor
- Isolated tremor consisting of bilateral upper limb action tremor, with no other significant motor abnormalities
- Greater than 3 years in duration
- With/without tremor in other locations (e.g. head, voice, trunk, lower limbs)
- Absence of other neurological signs (e.g. dystonia, ataxia, parkinsonism
What are signs of autonomic dysfunction
postural hypotension, constipation, abnormal sweating and sexual dysfunction
WHat is the first-line treatment for parkinsons if the motor symptoms are affecting the patient’s quality of life
levodopa
WHat is the first-line treatment for parkinsons if the motor symptoms are NOT affecting the patient’s quality of life
dopamine agonist or monoamine oxidase B (MAO-B) inhibitor
What are adverse side event of Dopamine receptor agonists
excessive sleepiness, hallucinations and impulse control disorders
Name an example of a Dopamine receptor agonists
Ropinirole
WHat are common SE of Levodopa
dyskinesia
dry mouth
anorexia
palpitations
postural hypotension
psychosis
What medication is Levodopa often combined with
peripheral decarboxylase inhibitors
Name 2 peripheral decarboxylase inhibitors
carbidopa and benserazide)
Why is Levodopa often combined with peripheral decarboxylase inhibitors
tops it from being metabolised in the body before it reaches the brain.
What are examples of Dyskinesia in levodopa users
- Dystonia (where excessive muscle contraction leads to abnormal postures or exaggerated movements)
- Chorea (abnormal involuntary movements that can be jerking and random)
- Athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)
How is dyskinesia associated with levodopa managed
Amantadine (glutamate antagonist)
What medication is used to extend the effective duration of the levodopa.
slow the breakdown of the levodopa in the brain
COMT Inhibitors (e.g., entacapone)
catechol-o-methyltransferase (COMT)
How do dopamine agonists work
mimic the action of dopamine in the basal ganglia, stimulating the dopamine receptors.
What are side effects of Dopamine agonists with prolonged use
Pulmonary fibrosis
Give an example of Dopamine agonists
Bromocriptine
Pergolide
Cabergoline
What do Monoamine oxidase enzymes do
break down neurotransmitters such as dopamine, serotonin and adrenaline.
What medication is used to delay/extend the use of levodopa
Dopamine agonists
Monoamine oxidase-B inhibitors
COMT Inhibitors
What are examples of Monoamine oxidase-B inhibitors
Selegiline
Rasagiline
How is Parkinson’s disease diagnosed
diagnosed clinically based on the history and examination findings.
UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.
What is Epilepsy
chronic neurological disorder characterised by recurrent, unprovoked seizures due to abnormal and excessive neuronal activity in the brain
What are the two general categorizations of epilepsy
- focal (originating from a specific region)
- or generalised (involving both hemispheres)
What are classifications of seizure types
tonic-clonic, absence, myoclonic, atonic, and tonic
What are causes of Epilepsy
- genetic predisposition
- structural brain abnormalities
- metabolic disorders
- immune conditions
- infectious diseases like meningitis or encephalitis
What is tonic
muscle tensing
What is clonic
muscle jerking
How do Generalised tonic-clonic seizures present generally
Before patients might experience aura
involve tonic (muscle tensing) and clonic (muscle jerking) movements associated with a complete loss of consciousness
After the seizure, there is a prolonged post-ictal period, where the person is confused, tired, and irritable or low.
What are associated symptoms with Generalised tonic-clonic seizures
tongue biting, incontinence, groaning and irregular breathing
Where do Partial seizures (or focal seizures) commonly occur
temporal lobe
affect hearing, speech, memory and emotions.
What symptoms are associated with temporal lobe focal seizures
- Often stay awake
- Déjà vu
- typically a rising epigastric sensation
- automatisms (e.g. lip smacking/grabbing/plucking)
What are DDx for seizures
Vasovagal syncope (fainting)
Pseudoseizures (non-epileptic attacks)
Cardiac syncope (e.g., arrhythmias or structural heart disease)
Hypoglycaemia
Hemiplegic migraine
Transient ischaemic attack
How do Myoclonic seizures present
sudden, brief muscle contractions, like an abrupt jump or jolt. They remain awake
How do Tonic seizures present
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.
How do Atonic seizures present
sudden loss of muscle tone, often resulting in a fall.
How do Absence seizures present
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.
How do Infantile spasms present
West syndrome
presents with clusters of full-body spasms
associated with developmental regression and has a poor prognosi
What is characteristic EEG finding of Infantile spasm
Hypsarrhythmia
WHat is treatment for infantile spasms
ACTH and vigabatrin
What are Febrile convulsions
tonic-clonic seizures that occur in children during a high fever
not caused by epilepsy
How is epilepsy investigated
electroencephalogram (EEG)
MRI brain -> structural pathology
What Additional investigations can be ordered for epilepsy
- ECG
- Serum electrolytes, including sodium, potassium, calcium and magnesium
- Blood glucose for hypoglycaemia and diabetes
- Blood cultures, urine cultures and lumbar puncture where sepsis, encephalitis or meningitis is suspected
What safety precautions can be taken for epilepsy
The DVLA will remove their driving licence until specific criteria are met (e.g., being seizure-free for one year)
Taking showers rather than baths (drowning is a major risk in epilepsy)
Particular caution with swimming, heights, traffic and dangerous equipment
What is first line management for male and non child bearing women with generalised tonic-clonic
Sodium valproate
What is first line management for male and non child bearing women with Partial (or focal)
Lamotrigine or Levetiracetam
What is first line management for male and non child bearing women with Myoclonic
Sodium valproate
What is first line management for male and non child bearing women with Tonic and atonic
Sodium valproate
What is first line management for male and non child bearing women with Absence
Ethosuximide
What is first line management for child bearing women with Generalised tonic-clonic
Lamotrigine or Levetiracetam
What is first line management for child bearing women with Partial (or focal)
Lamotrigine or Levetiracetam
What is first line management for child bearing women with Myoclonic
Levetiracetam
What is first line management for child bearing women with Tonic and atonic
Lamotrigine
What is first line management for child bearing women with Absence
Ethosuximide
How does Sodium Valproate work
increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brai
What are SE of Sodium Valproate
Teratogenic (harmful in pregnancy)
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility
What is Status Epilepticus
medical emergency defined as either:
- A seizure lasting more than 5 minutes
- Multiple seizures without regaining consciousness in the interim
What is the immediate management of status epilepticus
Securing the airway
Giving high-concentration oxygen
Checking blood glucose levels
Gaining intravenous access (inserting a cannula)
ABCDE approach
What is the Medical treatment of status epilepticus
- benzodiazepine - PR diazepam or buccal midazolam or IV lorezapam
- repeated benzodiazepine 5-10 minutes if the seizure continues
- (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
- general anaesthesia
What needs to be monitored in phenytoin
cardiac
What are benzodiazepine options for status epilepticus
Buccal midazolam (10mg)
Rectal diazepam (10mg)
Intravenous lorazepam (4mg)
What is cerebral palsy
non progressive permanent neurological problems resulting from damage to the brain around the time of birt
What are antenatal causes of cerebral palsy
- Maternal infections –> rubella, toxoplasmosis, CMV
- Trauma during pregnancy
- Placental abruption
- cerebral malformation
What are intrapartum causes of cerebral palsy
Birth asphyxia
Birth Trauma
Pre-term birth
What are postnatal causes of cerebral palsy
Meningitis
Severe neonatal jaundice
Head injury
intraventricular haemorrhage
what is spastic cerebral palsy
hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones
What are the 4 types of cerebral palsy
Spastic
Dyskinetic
Ataxic
Mixed
what is dyskinetic cerebral palsy
problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems.
This is the result of damage to the basal ganglia and the substantia nigra
what is ataxic cerebral palsy
problems with coordinated movement resulting from damage to the cerebellum
what is mixed cerebral palsy
a mix of spastic, dyskinetic and/or ataxic features
what is another name for Spastic CP
pyramidal CP
what is another name for Dyskinetic CP
athetoid CP and extrapyramidal CP.
What is Monoplegia CP
one limb affected
What is Hemiplegia CP
one side of the body affected
What is Diplegia CP
four limbs are affects, but mostly the legs
What is Quadriplegia CP
four limbs are affected more severely, often with seizures, speech disturbance and other impairments
What are signs and symptoms of cerebral palsy during development
Failure to meet milestones
Increased or decreased tone, generally or in specific limbs
Hand preference below 18 months is a key sign to remember for exams
Problems with coordination, speech or walking
Feeding or swallowing problems
Learning difficulties
What gait is associated commonly with CP
hemiplegic or diplegic gait
How does CP gait present
The leg will be extended with plantar flexion of the feet and toes.
This means they have to swing the leg around in a large semicircle when moving their leg from behind them to in front
How will CP present on examination
Like UMN lesion
good muscle bulk, increased tone, brisk reflexes and slightly reduced power
What are complications and associated conditions with CP
Learning disability
Epilepsy
Kyphoscoliosis
Muscle contractures
Hearing and visual impairment
Gastro-oesophageal reflux
What is the management for cerebral palsy
MDT team approach
Physiotherapy
Occupational therapy
Speech and language therapy
Dieticians
Orthopaedic surgeons
Paediatricians
Social workers
Charities and support groups
What medication can be involved in CP care
Muscle relaxants (e.g. baclofen) for muscle spasticity and contractures
Anti-epileptic drugs for seizures
Glycopyrronium bromide for excessive drooling
What is motor neuron disease
erm that encompasses a variety of specific diseases affecting the motor nerves.
progressive condition where eventually neurons stop working
What does motor neuron disease NOT affect
no effect on the sensory neurones.
Sensory symptoms suggest an alternate diagnosis.
Name two types of Motor Neurone Disease
amyotrophic lateral sclerosis - MC
progressive bulbar palsy - 2nd MC
progressive muscular atrophy
What are the bulbar muscles
muscles of talking and swallowing
What are RF for MND
FH
Smoking
heavy metals
pesticide
What is typical presentation of MND
late middle-aged (e.g., 60) man
insidious, progressive weakness of the muscles throughout the body, affecting the limbs, trunk, face and speech (dysarthria)
increased fatigue when exercising.
complain of clumsiness,
What are signs of lower motor neurone disease
Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes
What are signs of upper motor neurone disease
Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex
How is MND diagnosed
clinical
diagnosis of exclusion
What should MND show on nerve conduction study
normal motor conduction
How is MND managed
Riluzole –> can slow the progression of the disease and extend survival by several months in ALS.
Non-invasive ventilation (NIV)
PEG feedng tube
How can MND poatients be supported
Breaking bad news effectively and supportively
Multidisciplinary team (MDT) input to support and maintain their quality of life
Symptom control (e.g., baclofen for muscle spasticity and antimuscarinic medical for excessive saliva)
Benzodiazepines may help breathlessness worsened by anxiety
Advanced directives to document their wishes as the disease progresses
End-of-life care
How will most MND patients die
respiratory failure or pneumonia.
What is MND prognosis
50% of patients die within 3 years
What is multiple sclerosis
inflammatory demyelinating disease, clinically defined by two episodes of neurological dysfunction (brain, spinal cord or optic nerves) separated in space and time.
T4 autoimmune rxn
oligodendroctyes CNS
What cell myelinates nerves in the CNS
Oligodendrocytes in the central nervous system
What cell myelinates nerves in the PNS
Schwann cells in the peripheral nervous system
does Multiple sclerosis affect CNS or PNS
CNS
What does “disseminated in time and space” mean in MS
lesions vary in location, meaning that the affected sites and symptoms change over time
What factors influence MS
Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity
How do MS symptoms onset presents
Symptoms usually progress over more than 24 hours.
Symptoms tend to last days to weeks at the first presentation and then improve
What is Optic neuritis
demyelination of the optic nerve and presents with unilateral reduced vision, developing over hours to days.
WHat are key features of Optic neuritis
Central scotoma (an enlarged central blind spot)
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect
What are DDx for Optic neuritis
Neuromyelitis optica
Sarcoidosis
Systemic lupus erythematosus
Syphilis
Measles or mumps
Lyme disease
How is Optic neuritis managed
acute loss of vision –> urgent ophthalmology input.
treated with high-dose steroids.
MRI to monitor progression to MS
WHat is relative afferent pupillary defect
the pupil in the affected eye constricts more when shining a light in the contralateral eye than when shining it in the affected eye
How does optic neuritis when testing the direct pupillary reflex
reduced pupil response to shining light in the eye affected by optic neuritis.
However, the affected eye has a normal pupil response when testing the consensual pupillary reflex.
What focal weakness symptoms may MS present with
Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis
What focal sensory symptoms symptoms may MS present with
Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign
What is Lhermitte’s sign
electric shock sensation that travels down the spine and into the limbs when flexing the neck
What is affected in Lhermitte’s sign
cervical spinal cord in the dorsal column
What is Uhthoff sign
worsening of neurological function lasting less than 24 hours that can occur in multiple sclerosis patients due to increases in core body temperature
What is Sensory ataxia
due to loss of proprioception
What positive test does sensory ataxia result in
Romberg’s test
they lose balance when standing with their eyes closed)
Where would a lesion in MS causing sensory ataxia be located
dorsal columns
What is Cerebellar ataxia
problems with the cerebellum coordinating movement, indicating a cerebellar lesion
What are disease patterns in MS
Clinically isolated syndrome
Relapsing-remitting
Secondary progressive
Primary progressive
What is Clinically isolated syndrome MS
first episode of demyelination and neurological signs and symptoms. Patients with clinically isolated syndrome may never have another episode or may go on to develop MS
What is Relapsing-remitting MS
MC
episodes of disease and neurological symptoms followed by recovery
can be further classified based on whether the disease is active or worsening
What is Active Relapsing-remitting MS
new symptoms are developing, or new lesions are appearing on the MRI
What is Not Active Relapsing-remitting MS
no new symptoms or MRI lesions are developing
What is Worsening Relapsing-remitting MS
there is an overall worsening of disability over time
What is not Worsening Relapsing-remitting MS
there is no worsening of disability over time
What is Secondary progressive MS
where there was relapsing-remitting disease, but now there is a progressive worsening of symptoms with incomplete remissions.
What is Primary progressive MS
worsening disease and neurological symptoms from the point of diagnosis WITHOUT relapses and remission
How can progressive MS be further categorized
active or progressing
What investigations can support MS diagnosis
MRI scans can demonstrate typical lesions
Lumbar puncture can detect oligoclonal bands in the cerebrospinal fluid (CSF)
How can spasticity be managed in MS
Baclofen and gabapentin are first-line
What is the criteria is used to diagnose MS
McDonald criteria
What is McDonald criteria
≥ 2 clinical attacks desiminted in time and space and objective clinical evidence of ≥ 2 lesions
What is DDx for MS
Migraine
TIA Stroke
Giant Cell Arteritis
Fibromyalgia
Neuromyelitis optica
How is Acute relapse MS managed
High-dose steroids (e.g. oral or IV methylprednisolone)
oral 500mg
1g IV
What Disease modifying drugs are given for MS
natalizumab - 1st line
ocrelizumab
fingolimod
How can fatigue be managed in MS
modafinil or SSRI
How can Neuropathic pain be managed in MS
- amitriptyline
- duloxetine
- gabapentin
- pregabalin
How can urge incontinence be managed in MS
Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin
Who would be part of a specialist multidisciplinary team (MDT) for MS
including neurologists, specialist nurses, physiotherapists and occupational therapists.
Name two types of Muscular dystrophy
Duchennes muscular dystrophy
Beckers muscular dystrophy
Myotonic dystrophy
What is Gower’s Sign
Children with proximal muscle weakness use a specific technique to stand up from a lying position.
using their hands on their legs to help them stand up
What is Duchennes muscular dystrophy
defective gene for dystrophin on the X-chromosome
What is dystrophin
protein that helps hold muscles together at the cellular level.
Who is most affected by Duchennes muscular dystrophy boys or girls
boys
What is the inheritance pattern of Duchennes muscular dystrophy
X-linked recessive
If a mother is a carrier (meaning she has one faulty gene) of Duchennes muscular dystrophy and she has a child what is the chance of having the condition if she has a girl or boy
- 50% change of being a carrier if they female
- 50% change of having the condition if they are male
How does Duchennes Muscular Dystrophy present
present around 3 – 5 years with weakness in the muscles around their pelvis
delayed motor milestones
progressive to all muscles
calf pseudohypertrophy
symmetrical proximal muscle wasting
life expectance of around 25 – 35 years
How can Duchennes Muscular Dystrophy be managed pharmacuetically
Oral steroids have been shown to slow the progression of muscle weakness by as much as two years.
Creatine supplementation can give a slight improvement in muscle strength.
How is Duchennes Muscular Dystrophy diagnosed
genetic testing
GS muscle biopsy
What are complications of Duchennes Muscular Dystrophy
cardiomyopathy
heart failure
scoliosis
resp failure
What are Complications seen secondary to longterm corticosteroid use
osteoporosis
impaired glucose tolerance
obesity
Addisonian crisis triggered by suddenly stopping steroids or intercurrent illness
How is Muscular Dystrophy managed
occupational therapy, physiotherapy and medical appliances (such as wheelchairs and braces) as well as surgical and medical management of complications
What is Beckers muscular dystrophy
similar to Duchennes, however the dystrophin gene is less severely affected and maintains some of its function
When is typical presentation age for Beckers muscular dystrophy
Symptoms only start to appear around 8 – 12 years
wheelchair late 20s-30s
WHat is the difference between Beckers and Duchennes mutation
Duchennes = frameshift
Beckers = missense
What would bloods show for muscular dystrophy
inc CK
What does a patient that is unable to let go after shaking someones hand indicate
Myotonic dystrophy
What is key feature of myotonic dystrophy
prolonged muscle contraction.
WHat is the inheritance pattern of Huntington’s disease
autosomal dominant
WHat is Huntington’s disease
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.
autosomal dominant
what are other examples of trinucleotide repeat disorders
Fragile X syndrome
Spinocerebellar ataxia
Myotonic dystrophy
Friedrich ataxia
What does inheritance of Huntington’s display in successive generations
genetic anticipation
resulting in:
Earlier age of onset
Increased severity of disease
How does Huntington’s typically present initially
cognitive, psychiatric or mood problems
what movement disorders are associated with Huntington’s
- 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)
How is Huntington’s diagnosed
genetic testing
How is Huntington’s managed
- no treatment options
- Breaking bad news effectively and supportively
- Genetic counselling regarding relatives, pregnancy and children
- Multidisciplinary team (MDT) input to support and maintain their quality of life
- Physiotherapy to improve mobility, maintain joint function and prevent contractures
- Speech and language therapy where there are speech and swallowing difficulties
- Advanced directives to document their wishes as the disease progresses
- End-of-life care
What medication can be used for chorea symptoms
Tetrabenazine
What percent chance does a child of someone wth Huntington’s have to develop condition
50%
What is the prognosis of Huntington’s
Life expectance is around 10-20 years after the onset of symptoms
WHat is common cause of death in Huntington’s
aspiration pneumonia
Suicide
What are Migraines
complex neurological condition causing episodes or attacks of headache and associated symptoms
What are 4 types of Migraines
Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine
what factors influcence the pathophysiology of Migraines
combination of structural, functional, chemical, vascular and inflammatory factors.
What are the 5 stages of Migraine
- Premonitory or prodromal stage (can begin several days before the headache)
- Aura (lasting up to 60 minutes)
- Headache stage (lasts 4 to 72 hours)
- Resolution stage (the headache may fade away or be relieved abruptly by vomiting or sleeping)
- Postdromal or recovery phase
What are typical features of Migraine headaches
Usually unilateral but can be bilateral
Moderate-severe intensity
Pounding or throbbing in nature
Photophobia
Phonophobia
Osmophobia
Aura
Nausea and vomiting
what are typical visual symptoms of Migraine aura
Sparks in the vision
Blurred vision
Lines across the vision
Loss of visual fields (e.g., scotoma)
What is main feature of Hemiplegic Migraine
hemiplegia (unilateral limb weakness)
ataxia (loss of coordination) and impaired consciousnes
what are causes of Hemiplegic Migraine
Familial hemiplegic migraine is an autosomal dominant
what are DDx for Hemiplegic Migraine
stroke or TIA.
What are Migraine triggers
Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma
What is acute management of Migraine
Triptans (e.g., sumatriptan)
NSAIDs (e.g., ibuprofen or naproxen)
Paracetamol
Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)
what is Migraine prophylactic medication
Propranolol (a non-selective beta blocker)
Amitriptyline (a tricyclic antidepressant)
Topiramate (teratogenic and very effective contraception is needed)
What class of medication is Triptans
5-HT receptor agonists (they bind to and stimulate serotonin receptors
What are the mechanisms of action of Triptans
Cranial vasoconstriction
Inhibiting the transmission of pain signals
Inhibiting the release of inflammatory neuropeptides
What is a common side-effect of triptan use
Tightness of the throat and chest
What are DDx for headache
Tension headaches
Migraines
Cluster headaches
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Venous sinus thrombosis
Subarachnoid haemorrhage
Medication overuse
Hormonal headache
Cervical spondylosis
Carbon monoxide poisoning
Trigeminal neuralgia
Raised intracranial pressure
Brain tumours
Meningitis
Encephalitis
Brain abscess
Pre-eclampsia
What could Fever, photophobia or neck stiffness headache indicate
meningitis, encephalitis or brain abscess
What could New neurological symptoms with headache indicate
haemorrhage or tumours
What could Visual disturbance with headache indicate
giant cell arteritis, glaucoma or tumours
What could Sudden-onset occipital headache indicate
subarachnoid haemorrhage
What could headache Worse on coughing or straining indicate
raised intracranial pressure
What could Vomiting with headache indicate
raised intracranial pressure or carbon monoxide poisoning
What could Postural, worse on standing, lying or bending over headache indicate
raised intracranial pressure
What could History of trauma with headache indicate
intracranial haemorrhage
What could History of cancer with headache indicate
brain metastasis
what could headache with pregnancy indicate
pre-eclampsia)
What does Papilloedema suggest
raised intracranial pressure, which may be due to a brain tumour, benign intracranial hypertension or an intracranial bleed.
What are tension headaches
cause a mild ache or pressure in a band-like pattern around the head. They develop and resolve gradually and do not produce visual changes.
What may tension headaches be associated with
Stress
Depression
Alcohol
Skipping meals
Dehydration
how are tension headaches managed
Reassurance
Simple analgesia (e.g., ibuprofen or paracetamol)
What is first line medication for chronic or frequent tension headache
Amitriptyline
what is Sinusitis
inflammation of the paranasal sinuses
How does Sinusitis present
causes pain and pressure following a recent viral upper respiratory tract infection. There may be tenderness and swelling on palpation of the affected areas.
What is first line treatment for Sinusitis
Most cases are caused by a viral infection and resolve within 2-3 weeks.
Prolonged cases (over 10 days) may be treated with a steroid nasal spray or antibiotics (phenoxymethylpenicillin first-line).
What is Hormonal Headache
related to low oestrogen.
When do hormonal headaches occur
Two days before and the first three days of the menstrual period
In the perimenopausal period
Early pregnancy (headaches in the second half of pregnancy should prompt investigations for pre-eclampsia)
How are Hormonal Headache treated
NSAIDS (e.g., mefenamic acid) and triptans
WHat are features of Hormonal Headache
similar features to migraines, with a unilateral, pulsatile headache associated with nausea
What is Trigeminal Neuralgia
excruciating shooting or stabbing facial pain followed by a burning ache.
It is caused by either neurovascular compression from a neighboring vessel or nerve damage resulting from an underlying condition such as multiple sclerosis.
WHat are the three branches of the Trigeminal nerve
Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)
what can trigger Trigeminal Neuralgia
touch, taking, eating, shaving or cold. Attacks may worsen over time.
What is first line medication for Trigeminal Neuralgia
carbamazepine
What are Cluster headaches
Severe and unbearable unilateral headaches, usually centred around the eye.
What is the frequency of Cluster headaches
come in clusters of attacks and then disappear for extended periods.
clusters typically last 4-12 weeks
Attacks last between 15 minutes and 3 hours.
What are triggers to Cluster headaches
alcohol, strong smells or exercise
What are Cluster headache associated symptoms
Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating
How are acute Cluster headaches managed
Triptans (e.g., subcutaneous or intranasal sumatriptan)
High-flow 100% oxygen (may be kept at home)
What is prophylaxis for Cluster headaches
1st line = Verapamil
alt
Occipital nerve block
Prednisolone (e.g., a short course to break the cycle during clusters)
Lithium
What is Giant cell arteritis (GCA)
aka temporal arteritis. It is a type of systemic vasculitis affecting the medium and large arteries.
What is Giant cell arteritis strongly linked to
polymyalgia rheumatica.
older white patients.
How does Giant cell arteritis present
Unilateral headache severe and around the temple and forehead.
Scalp tenderness (e.g., noticed when brushing the hair)
Jaw claudication
Blurred or double vision
Loss of vision if untreated
How may Giant cell arteritis present on examination
temporal artery may be tender and thickened to palpation, with reduced or absent pulsation.
What are associated features with Giant cell arteritis
Symptoms of polymyalgia rheumatica (e.g., shoulder and pelvic girdle pain and stiffness)
Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
Muscle tenderness
Carpel tunnel syndrome
Peripheral oedema
How is Giant cell arteritis investigated
Clinical presentation
Raised inflammatory markers, particularly ESR (usually more than 50 mm/hour)
Temporal artery biopsy
Duplex ultrasound
In giant cell arteritis occlusion of what artery causes anterior ischemic optic neuropathy
posterior ciliary artery
How does Giant cell arteritis present on biposy
showing multinucleated giant cells
skip lesions
How does Giant cell arteritis present on US
showing the hypoechoic “halo” sign and stenosis of the temporal artery
How does Giant cell arteritis present on Fundoscopy
swollen pale disc and blurred margins
How is Giant cell arteritis initially managed
steroids started before Dx to reduce risk of vision loss
- 40-60mg prednisolone daily with no visual symptoms or jaw claudication
- 500mg-1000mg methylprednisolone daily with visual symptoms or jaw claudication
What medication is involved in Giant cell arteritis management longer term
steroids weaned over 1-2 years
Aspirin 75mg daily decreases vision loss and strokes
Proton pump inhibitor (e.g., omeprazole) for gastroprotection while on steroids
Bisphosphonates and calcium and vitamin D for bone protection while on steroids
What people may be involved in management of Giant cell arteritis
Rheumatology for specialist diagnosis and management
Vascular surgeons for a temporal artery biopsy
Ophthalmology review for visual symptoms
WHat are complications of Giant cell arteritis
Visual loss ** = irreversible
Steroid-related complications (e.g., weight gain, diabetes and osteoporosis)
Cerebrovascular accident (stroke)
WHat is Myasthenia gravis
autoimmune condition affecting the neuromuscular junction. It causes muscle weakness that progressively worsens with activity and improves with rest.
who does Myasthenia gravis typically affect
ffecting women under 40 and men over 60.
What is the pathophysiology of Myasthenia gravis
Acetylcholine stimulates muscle contraction
Acetylcholine receptor (AChR) antibodies in MG
bind to the postsynaptic acetylcholine receptors, blocking them and preventing stimulation by acetylcholine
more the receptors are used during muscle activity, the more they become blocked.
How does Myasthenia gravis present
weakness that worsens with muscle use and improves with rest
Difficulty climbing stairs, standing from a seat or raising their hands above their head
diplopia
ptosis
facial weakness
jaw fatigue
weak swallow
Slurred speech
What part of the body does Myasthenia gravis most affect
affect the proximal muscles of the limbs and small muscles of the head and neck, with:
What ways can Myasthenia gravis symptoms be elicited
Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
What further examination steps can be taken in Myasthenia gravis
Checking for a thymectomy scar
Testing the forced vital capacity (FVC)
What condition is Myasthenia gravis strongly linked with
- thymomas (thymus gland tumours)
- 10-20% of patients with myasthenia gravis have a thymoma.
- 30% of patients with a thymoma develop myasthenia gravis.
- autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
- thymic hyperplasia in 50-70%
What do antibody tests for Myasthenia gravis look for
AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)
What further investigations can be down for Myasthenia gravis
A CT or MRI of the thymus gland is used to look for a thymoma.
The edrophonium test can be helpful where there is doubt about the diagnosis.
What is a edrophonium test for Myasthenia gravis
Patients are given intravenous edrophonium chloride
Edrophonium blocks enzymes in the neuromuscular junction that break down acetylcholine = level of acetylcholine at the neuromuscular junction rises, temporarily relieving the weakness
How is Myasthenia gravis treated
- Pyridostigmine a long acting acetylcholinesterase 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
What is a Myasthenic crisis
life-threatening complication of myasthenia gravis
often triggered by another illness
Respiratory muscle weakness can lead to respiratory failure.
How is Myasthenic crisis treated
non-invasive ventilation or mechanical ventilation.
Treatment is with IV immunoglobulins and plasmapheresis.
What is Guillain-Barré Syndrome
acute paralytic polyneuropathy that affects the peripheral nervous system
acute, symmetrical, ascending weakness and can also cause sensory symptoms.
What is Guillain-Barré Syndrome associated with
Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).
What is pathophysiology of Guillain-Barré Syndrome
molecular mimicry
target proteins on the myelin sheath or the nerve axon of PNS
How does Guillain-Barré Syndrome present
Symptoms within four weeks of the triggering infection
begin in the feet and progress upward.
The characteristic features are:
Symmetrical ascending weakness
Reduced reflexes
peripheral loss of sensation
neuropathic pain
How is Guillain-Barré Syndrome diagnosed
clinically with Brighton criteria suppoted by nerve conduction study and LP
anti-GM1 antibodies
What would Guillain-Barré Syndrome show on nerve conduction studies
showing reduced signal through the nerves
WHat would Guillain-Barré Syndrome show on lumbar puncture
showing raised protein with a normal cell count and glucose
How is Guillain-Barré Syndrome managed
- Supportive care
- VTE prophylaxis
- IV immunoglobulins (IVIG) first-line
- Plasmapheresis is an alternative to IVIG
with respiratory failure may require intubation, ventilation and admission to the intensive care unit.
How is main complication of Guillain-Barré Syndrome
pulmonary embolism is a leading cause of death
What is prognosis for Guillain-Barré Syndrome
Recovery can take months to year
Most full recovery
Some are left with significant disability
Mortality is around 5%
What is Peripheral Neuropathy
reduced sensory and motor function in the peripheral nerves, typically affecting the feet and hands (“stocking-glove” distribution).
What are causes of Peripheral Neuropathy
A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis
What does facial nerve pass through
temporal bone and parotid gland.
What are 5 branches of the facial nerve
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
WHat is the motor function of the facial nerve
Facial expression
Stapedius in the inner ear
Posterior digastric, stylohyoid and platysma muscles
what is the sensory function fo the facial nerve
taste from the anterior 2/3 of the tongue.
what si the parasympathetic supply of the facial nerve
Submandibular and sublingual salivary glands
Lacrimal gland (stimulating tear production)
How is UMNv LMN lesion distingiushed
UMN= stroke
LMN= palsy
UMN = forehead spared = move forehead
When do Bilateral upper motor neurone lesions occur
Cerebrovascular accidents (strokes)
Tumours
when do unilater upper motor neurone lesions occur
Pseudobulbar palsies
Motor neurone disease
how is bells palsy treated
if within 72 hours of developing symptoms: prednisolone
50mg for 10 days
60mg for 5 days followed by a 5-day reducing regime, dropping the dose by 10mg per day
+ lubricating eye drops
What is Ramsay-Hunt syndrome
caused by the varicella zoster virus (VZV).
How does Ramsay-Hunt syndrome present
- unilateral LMN facial nerve palsy.
- painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side.
How is Ramsay-Hunt syndrome treated
aciclovir and prednisolone. Patients also require lubricating eye drops.
What are Systemic disease causes of LMN facial nerve palsy
Diabetes
Sarcoidosis
Leukaemia
Multiple sclerosis
Guillain–Barré
What are tumor causes of LMN facial nerve palsy
Acoustic neuroma
Parotid tumour
Cholesteatoma
What are benign brain tumors
meningiomas
what are malignant brain tumors
glioblastomas
How do brain tumors present
progressive focal neurological symptoms
symptoms and signs of raised intracranial pressure (intracranial hypertension)
What are causes of raised ICP
Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection
What are symptoms of raised ICP
Constant headache
Nocturnal (occurring at night)
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
Papilloedema on fundoscopy
What are signs of raised ICP
Altered mental state
Visual field defects
Seizures (particularly partial seizures)
Unilateral ptosis (drooping upper eyelid)
Third and sixth nerve palsies
What is Papilloedema
swelling of the optic disc secondary to raised intracranial pressure.
How does Papilloedema present on fundoscopy
Blurring of the optic disc margin
Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
Loss of venous pulsation
Engorged retinal veins
Haemorrhages around the optic disc
Paton’s lines, which are creases or folds in the retina around the optic disc
How do retinal vessels cross disc in Papilloedema
Vessels can travel straight across a flat surface, whereas they will curve over a raised disc.
What are gliomas tumors of
glial cells in the brain or spinal cor
What are types of Glial cells
astrocytes, oligodendrocytes and ependymal cells
what are three main tyoes of Gliomas
Astrocytoma (the most common and aggressive form is glioblastoma)
Oligodendroglioma
Ependymoma
is a grade 1 Gliomas most benign or malignant
benign
What cells do meningiomas grow from
meninges
What cancers spread to brain
Lung
Breast
Renal cell carcinoma
Melanoma
What visual field defect do pit tumors cause
bitemporal hemianopia, with loss of the outer half of the visual fields in both eyes.
WHat hormones conditions can Pituitary Tumours cause
Acromegaly (excessive growth hormone)
Hyperprolactinaemia (excessive prolactin)
Cushing’s disease (excessive ACTH and cortisol)
Thyrotoxicosis (excessive TSH and thyroid hormone)
How can Pituitary Tumours be managed
Trans-sphenoidal surgery (through the nose and sphenoid bone)
Radiotherapy
Bromocriptine to block excess prolactin
Somatostatin analogues (e.g., octreotide) to block excess growth hormone
What are Acoustic Neuroma
tumor of schwann cells that surround the auditory nerve (vestibulocochlear nerve) that innervates the inner ear.
provide myelin sheath of PNS
what is another name for Acoustic neuromas
vestibular schwannomas.
What angle do Acoustic Neuroma occur are
and what is the investigation of choice
cerebellopontine angle
Ix = MRI of the cerebellopontine angle
What are bilateral Acoustic Neuroma associated with
neurofibromatosis type 2.
How do Acoustic Neuroma present
Unilateral sensorineural hearing loss (often the first symptom)
classic combination of vertigo, hearing loss, tinnitus and an absent corneal reflex.
Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)
How are Acoustic Neuroma managed
Conservative management with monitoring may be used if there are no symptoms or treatment is inappropriate
Surgery to remove the tumour (partial or total removal)
Radiotherapy to reduce the growth
What is 1st line investigation in patients with possible brain tumor
MRI brain
How is the definitive diagnosis of brain tumors given
Biopsy
definitive histological diagnosis,
What are treatment options for brain tumors
Surgery
Chemotherapy
Radiotherapy
Palliative care
What is Stevens-Johnson syndrome and and toxic epidermal necrolysis (TEN)
spectrum of disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of ski
What is difference between SJS and TEN
SJS affects less that 10% of body surface area whereas TEN affects more than 10% of body surface area.
What medication causes SJS
Anti-epileptics
Antibiotics
Allopurinol
NSAIDs
what infections causes SJS
Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV
How does SJS present
non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin. They then develop a purple or red rash that spreads across the skin and starts to blister.
How is SJS managed
medical emergencies
cease medication stat
IV fluids
steroids, immunoglobulins and immunosuppressant
What are complications of SJS
secondary infection
permanent skin damage
visual complications
what is Neurofibromatosis
genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system
enign but can cause neurological and structural problems.
what is MC Neurofibromatosis
type 1
Where is the gene for Neurofibromatosis type 1 found
chromosome 17.
what does Neurofibromatosis gene code for
neurofibromin
tumour suppressor protein.
what is the inheritance pattern of Neurofibromatosis
auto dom
What is the diagnostic criteria for Neurofibromatosis type 1
C – Café-au-lait spots (more than 15mm diameter is significant in adults)
R – Relative with NF1
A – Axillary or inguinal freckling
BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
N – Neurofibromas
G – Glioma of the optic pathway
CRABBING
How is Neurofibromatosis managed
iagnostic criteria. Genetic testing can be helpful.
no treatment
What are complications of Neurofibromatosis type 1
- malignant peripheral nerve sheath (MPNST)
- gastrointestinal stromal tumours (GIST).
- Migraines
- Epilepsy
- Renal artery stenosis, causing hypertension
- Learning disability
- Behavioural problems (e.g., ADHD)
- Scoliosis of the spine
- Vision loss (secondary to optic nerve gliomas)
- Brain tumours
- Spinal cord tumours with associated neurology (e.g., paraplegia)
- Increased risk of cancer (e.g., breast cancer and leukaemia)
where is the gene for Neurofibromatosis type 2 located
chromosome 22
what does the affected gene in Neurofibromatosis type 2 code for
merlin, a tumour suppressor protein important in Schwann cells
what is Neurofibromatosis type 2 associated with
acoustic neuromas, which are tumours of the auditory nerve that innervates the inner ear.
What does a palsy in the third cranial nerve (the oculomotor nerve) cause
Ptosis (drooping upper eyelid)
Dilated non-reactive pupil
Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye
the 3rd cranial nerve supplies all extraocular muscles except …
lateral rectus and superior oblique
What does a third nerve palsy that does not affect the pupil (sparing of the pupil) suggest
microvascular… parasympathetic fibres are spared.
Diabetes
Hypertension
Ischaemia
what can cause a full third nerve palsy
- Vasulitis
- DM
- Cavernous sinus thrombosis
- Posterior communicating artery aneurysm –> Painful CN3
- Raised intracranial pressure –> causung trans-tentorial, or uncal, herniation.
- Weber’s syndrome:
what is horner sydnrome triad
Ptosis
Miosis
Anhidrosis (loss of sweating)
in horners syndrome what does anhidrosis of the arm, trunk and face indicate
Central lesions (occurring before the nerves exit the spinal cord)
what causes horners sydnrome
damage to the sympathetic nervous system supplying the face.
in horners syndrome what does anhidrosis of the face indicate
Pre-ganglionic lesions
what are central lesion causes of horners syndrome
Central lesions:
S – Stroke
S – Multiple Sclerosis
S – Swelling (tumours)
S – Syringomyelia (cyst in the spinal cord)
what are Pre-ganglionic lesion causes of horners syndrome
T – Tumour (Pancoast tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib and clavicle)
what are post-ganglionic lesion causes of horners syndrome
C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache
what is Argyll-Robertson Pupil
neurosyphilis
it accommodates but does not react
causes of dilated pupil
Congenital
Stimulants (e.g., cocaine)
Anticholinergics (e.g., oxybutynin)
Trauma
Third nerve palsy
Holmes-Adie syndrome
Raised intracranial pressure
Acute angle-closure glaucoma
causes of constricted pupil
Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine
What is Meningitis
inflammation of the meninges, the lining of the brain and spinal cord.
What are causes of bacterial Meningitis
Neisseria meningitidis
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae
Group B streptococcus (GBS) (particularly in neonates as GBS may colonise the vagina)
Listeria monocytogenes (particularly in neonates)
What type of bacteria is Neisseria meningitidis
gram-negative diplococcus bacteria
what is Meningococcal septicaemia
meningococcus bacterial infection is in the bloodstream
(non blanching rash)
what is Meningococcal meningitis
bacteria infects the meninges and the cerebrospinal fluid.
what are mc causes of viral Meningitis
Enteroviruses (e.g., coxsackievirus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)
how is viral Meningitis tested
Viral PCR testing
how is Herpes simplex virus (HSV) and Varicella zoster virus (VZV) Meningitis treated
Aciclovir
How does Meningitis present
Fever
Neck stiffness
Vomiting
non-blanching rash
Headache
Photophobia
Altered consciousness
Seizures
What non specific symptoms can babies and neonates with Meningitis present with
hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle
What are the special tests to do for Meningitis
Kernig’s test
Brudzinski’s test
what is Kernig’s test
A positive test is the elicitation of pain or resistance with passive extension of the patient’s knee
what is Brudzinski’s test
Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed
where is needle inserted for lumbar puncture
L3-L4 or L4/L5 intervertebral space
what would CSF sample for bacterial Meningitis show
Appearance = cloudy
Protein = high
Glucose = low
WCC = high neutrophils
Culture = bacteria
what would CSF sample for viral Meningitis show
Appearance = clear
Protein = mild to normal
Glucose = normal
WCC = high lymphocytes
Culture = negative
How is Meningitis managed in GP
benzylpenicillin (IM or IV)
Under 1 year – 300mg
1-9 years – 600mg
Over 10 years – 1200mg
How is Meningitis managed in hospital
Under 3 months – cefotaxime plus amoxicillin (amoxicillin is to cover listeria)
Above 3 months – ceftriaxone
how are close contacts of Meningitis treated
single dose of ciprofloxacin
What should be added to Meningitis treatemnt if risk of penicillin-resistant pneumococcal infection
Vancomycin
Is Meningitis a notifiable disease
yes
What are complications of Meningitis
Hearing loss (a key complication)
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits, such as limb weakness or spasticity
what can be given to prevent hearing loss with Meningitis
Steroids (e.g., dexamethasone) a
When is LP contraindicated
- signs of raised ICP
- GCS below 9
- haemodynamically unstable
- active seizures or post-ictal.
What investigations can be ordered for meningitis
blood cultures and a lumbar puncture
what is Encephalitis
inflammation of the brain. This can be the result of infective or non-infective causes
NI = autoimmune
what is the MC cause of Encephalitis
herpes simplex virus (HSV).
type 1 in children (cold sores)
type 2 in neonates (genital herpes)
how does Encephalitis present
- fever, headache, psychiatric symptoms, seizures, vomiting
- focal features e.g. aphasia
what are lab investigations for Encephalitis
Lumbar puncture, sending cerebrospinal fluid for viral PCR
Blood tests
Serology
Autoimmune antibody panel
what is imaging investigation of chocie for Encephalitis
CT or MRI scan (better)
areas of inflammation or oedema
What does imaging for HSV encephalitis show
temporal lobe changes (hypodensities on CT, or hyperintensities on MRI) and bilateral temporal lobe changes
How is Encephalitis managed
- IV Aciclovir treats herpes simplex virus (HSV) and varicella zoster virus (VZV)
- IV Ganciclovir treat cytomegalovirus (CMV)
what are complications of Encephalitis
Lasting fatigue and prolonged recovery
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance
How does brain abscess present
headache
focal neurological deficits
fever
signs of raised ICP
how is brain abscess diagnosed
GS = MRI
CT for detetcing complications
needle aspiration
How is brain abscess managed
IV antibiotics: IV 3rd-generation cephalosporin (ceftriaxone) + metronidazole
drainage or debridement
ICP management = dexamethasone
What causes brain abscess
contiguous spread of infection from sinusitis, otitis media, or dental infections
haematogenous spread from distant sources (e.g., endocarditis, pulmonary infections)
direct inoculation from trauma or neurosurgical procedures.
What are the complications of a brain abscess
seizures, meningitis, ventriculitis, hydrocephalus, cerebral oedema, and herniation
What is hydrocephalus
cerebrospinal fluid (CSF) building up abnormally within the brain and spinal cord.
This is a result of either over-production of CSF or a problem with draining or absorbing CSF.
where is CSF created
created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles
where is CSF absorbed
into the venous system by the arachnoid granulations.
WHat are the 4 ventricles in the brain
two lateral ventricles, the third and the fourth ventricles
What is the MC cause of hydrocephalus
aqueductal stenosis
cerebral aqueduct that connects the third and fourth ventricle is stenosed (narrowed).
causing CSF to build up in the lateral and third ventricles.
What are other causes of hydrocephalus
- Arachnoid cysts can block the outflow of CSF if they are large enough
- Arnold-Chiari malformation is where the cerebellum herniates downwards through the foramen magnum, blocking the outflow of CSF
- Chromosomal abnormalities and congenital malformations can cause obstruction to CSF drainage.
how is Normal pressure hydrocephalus investigated
CT
hydrocephalus with an enlarged fourth ventricle
in addition to the ventriculomegaly there is typically an absence of substantial sulcal atrophy
How does Normal pressure hydrocephalus present
- urinary incontinence
- dementia and bradyphrenia (slow thinking)
- gait abnormality (may be similar to Parkinson’s disease)
what is Normal pressure hydrocephalus associated with
subarachnoid haemorrhage or meningitis
How is hydrocephalus treated
Ventriculoperitoneal Shunt
CSF from the ventricles into another body cavity Usually the peritoneal cavity i
what are complications of VP shunts
- Intraventricular haemorrhage during shunt related surgery
- Infection
- Blockage
- Excessive drainage
- Outgrowing them (they typically need replacing around every 2 years as the child grows)
What is Hypoxic-ischaemic encephalopathy
neurological condition resulting from inadequate cerebral oxygen supply.
WHat is primary energy failure in Hypoxic-ischaemic encephalopathy
occurs immediately during the hypoxic-ischaemic event, leading to anaerobic metabolism, lactic acidosis, and cytotoxic oedem
what is secondary energy failure in Hypoxic-ischaemic encephalopathy
ccurring hours to days later, is characterised by renewed accumulation of toxic metabolites and free radicals causing further neuronal death
How does Hypoxic-ischaemic encephalopathy present
- altered consciousness levels ranging from lethargy to coma
- seizures
- abnormal tone and reflexes.
How is Hypoxic-ischaemic encephalopathy managed
supportive care such as maintaining normal body temperature and blood glucose levels alongside seizure control.
therapeutic hypothermia
What are causes of Hypoxic-ischaemic encephalopathy
- Maternal shock
- Intrapartum haemorrhage
- Prolapsed cord, causing compression of the cord during birth
- Nuchal cord, where the cord is wrapped around the neck of the baby
How is Hypoxic-ischaemic encephalopathy investiagted
Blood gas analysis
complete blood count
serum electrolytes and glucose
LFT
US = 1st line
MRI = GS
How is Hypoxic-Ischaemic Encephalopathy Graded
Sarnat Staging
WHat is Ménière’s disease
long-term inner ear disorder that causes recurrent attacks of vertigo
What is Ménière’s disease triad
Hearing loss
Vertigo
Tinnitus
How is Ménière’s disease diagnosed
clinical, based on the signs and symptoms
ENT
audiology assessment
How are acute Ménière’s disease attacks managed
acute attacks: buccal or intramuscular prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
What is Ménière’s disease prophylaxis
Betahistine
what causes Ménière’s disease
excessive buildup of endolymph in the labyrinth of the inner ear, causing a higher pressure than normal and disrupting the sensory signal
WHat are features of Wernicke’s encephalopathy
Confusion
Ataxia
Nystagmus
Ophthamoplegia
PEripheral
Neuropathy
WHat are features of Korsakoff syndrome
- anterograde amnesia: inability to acquire new memories
- retrograde amnesia
- confabulation
how is Wernicke’s encephalopathy treated
IV thiamine
what is Cauda Equina
surgical emergency where the nerve roots of the cauda equina at the bottom of the spine are compressed
What is the sensory supply of the Cauda Equina
lower limbs, perineum, bladder and rectum
What is the motor supply of the Cauda Equina
lower limbs and the anal and urethral sphincters
What is the parasympathetic supply of the Cauda Equina
bladder and rectum
what are causes of cauda equina
Herniated disc (the most common cause)
Tumours, particularly metastasis
Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
Abscess (infection)
Trauma
What are red flag signs of cauda equina
- Saddle anaesthesia (loss of sensation in the perineum – around the genitals and anus)
- Loss of sensation in the bladder and rectum (not knowing when they are full)
- Urinary retention or incontinence
- Faecal incontinence
- Bilateral sciatica
- Bilateral or severe motor weakness in the legs
- Reduced anal tone on PR examination
How is cauda equina investigated
Emergency MRI scan to confirm or exclude cauda equina syndrome
how is cauda equina managed
lumbar decompression surgery
how can cauda equina be differentiated from metastatic spinal cord compression
cauda equina = LMN signs(reduced tone and reflexes)
MSSC = UMN signs (inc tone, reflxes and plantar reflex
How is metastatic spinal cord compression managed
High dose dexamethasone (to reduce swelling in the tumour and relieve compression)
Analgesia
Surgery
Radiotherapy
Chemotherapy
What makes MSSC pain worse
worse on coughing or straining.
what is Anterior Cord Syndrome
Damage to the anterior part of the spinal cord resulting in
LOSS of motor function and pain and temperature sensation,
but preservation of proprioception and touch.
what are signs of autonomic dysreflexia
severe hypertension and flushing and sweating above the level of injury
full bladder
can only occur if the spinal cord injury occurs above the T6 level
what causes autonomic dysreflexia
spinal cord injury at, or above T6
MC triggered by faecal impaction or urinary retention
what is Syringomyelia
cyst or cavity forms within the spinal cord leading to collection of CSF within the spinal cord.
how does Syringomyelia present
cape-like loss of pain and temperature sensation
due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine
what are complications of spinal injuries
pressure sores, urinary tract infections, deep vein thrombosis and autonomic dysreflexia
what is Brown-Séquard Syndrome
damage to one half of the spinal cord.
- ipsilateral weakness below lesion
- ipsilateral loss of proprioception and vibration sensation
- contralateral loss of pain and temperature sensation
What is malaria
disease caused by Plasmodium protozoa which is spread by the female Anopheles mosquito
name 3 types of malaria
- Plasmodium falciparum (the most common and severe form)
- Plasmodium vivax
- Plasmodium ovale
- Plasmodium malariae
*
what is dormnat malaria called
hypnozoites
where do malaria mature
liver
what is malaria travelling in RBc called
merozoites
when merozoites rupture RBc what dot hey cause
haemolytic anaemia.
what are malaria symptoms
Fever (up to 41ºC) with sweats and rigors
Fatigue
Myalgia (muscle aches and pain)
Headache
Nausea
Vomiting
what are malaria signs on examination
Pallor due to the anaemia
Hepatosplenomegaly
Jaundice (bilirubin is released during the rupture of red blood cells)
how is malaria investigated
malaria blood film
schizonts on a blood film
what is required to exclude a malaria diagnosis
Three negative samples taken over three consecutive
how is uncomplicated malaria managed
1st - oral artemisinin-based combination therapies
eg artemether plus lumefantrine
artesunate plus amodiaquine
how is severe malaria manahed
1st - IV Artesunate is the usual first choice (haemolysis is a common side effect)
what are complications of malaria
Cerebral malaria
Seizures
Reduced consciousness
Acute kidney injury
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death
what is antimalarial medication with least side effects
Proguanil / atovaquone (Malarone)
