Neuro flashcards
Transient ischemic attack
RF
Pathology
Symptoms
Investigations
Treatments
A transient sudden onset of focal neurological deficit that may last from a few minutes to 24 hours, WITHOUT INFARCTION. (most patients have complete resolution of symptoms within 1 hour)
RF - (mostly like IHD), smoking, T2DM, hypertension, Atrial fibrillation, valvular disease, carotid stenosis, intracranial stenosis
PATHOLOGY
Caused mainly by carotid thrombi-emboli (90% ICA, 10% vertebral arteries) –> leading to ischaemia
Symptoms depend on which artery the blockage has occurred in.
SYMPTOMS
ACA
- Contralateral hemiparesis and sensory loss (more lower limb for Anterior cerebral)
MCA
- Weak numb contralateral side of body, face drooping with forehead spread, dysphasia
PCA
- Contralateral homonymous hemianopia with macular sparing
Ophthalmic/retinal artery = Amaurosis fugax
Vertebral
- Cerebellar syndrome- DANISH
- Brainstem - CN lesions 3-12
INVESTIGATIONS
Clinically made
Tools
- FAST (Face, Arms, Speech, Time)
IMAGING OF CHOICE - Diffusion weighted MRI scan (determine territory of ischaemia)
(don’t use CT for TIA)
TREATMENT
1st line - aspirin 300mg unless contraindicated (immediately)
- then refer for specialist assessment within 24 hours
Secondary prevention: Can give clopidogrel (antiplatelet) and atorvastatin (statin) - for long term prophylaxis
Ischaemic stroke + haemorrhagic stroke
RF
Pathology
Symptoms
Investigations
Treatments
Focal neurological deficit lasting more than 24 hours with infarction
RF - Hypertension, Older age, family history, history of stroke/TIA,
PATHOLOGY
Ischaemic stroke (85%) - Caused by vascular occlusion or stenosis
- Carotid thrombo-emboli
- (Basically a very long TIA)
Haemorrhagic stroke (15%) - Caused by vascular rupture leading to a haemorrhage
- Can be due to trauma, hypertension, berry aneurysm rupture
- Assume haemorrhagic stroke if patient is on anticoagulants unless proven otherwise
SYMPTOMS
ACA
- Contralateral hemiparesis and sensory loss (more lower limb for Anterior cerebral)
MCA
- Weak numb contralateral side of body, face drooping with forehead spread, dysphasia
PCA
- Contralateral homonymous hemianopia with macular sparing
Ophthalmic/retinal artery = Amaurosis fugax
Vertebral
- Cerebellar syndrome- DANISH
- Brainstem - CN lesions 3-12
Possible to get lacunar strokes (a common type of ischaemic stroke) of lenticulostriate arteries (supplying deep brain arteries) –> Pure motor hemiparesis, ataxic hemiparesis
INVESTIGATIONS
1st line - Urgent Non contrast CT of the head (differentiates between ischaemic/haemorrhagic stroke - appears as hyperdense blood)
Tools
- FAST (Face, Arms, Speech, Time)
- ROSIER tool (recognition of stroker in emergency room)
TREATMENT
Ischaemic stroke (treatment within 4.5 hours and intracranial haemorrhage has been excluded)
1st line - Alteplase (IV) - Clot buster (thrombolysis)
(if it is after 4.5-6 hours of symptom onset –> offer thrombectomy
+ Plus –> Aspirin 300mg for 2 weeks
and then clopidogrel for rest of life
Haemorrhagic stroke –> Immediate neurosurgery referral (+ supportive care - oxygen, BP, temperature)
Common places for berry aneurysms
- Junction of the anterior communicating artery and anterior cerebral artery
- Junction of the posterior communicating artery with the internal carotid artery
- Bifurcation of the middle cerebral artery
Layers from the skull to the brain
Skull (bony structure that encases and protects the brain)
Dura mater (outermost layer of the meninges - adheres closely to the inner surface of the skull)
Arachnoid mater (separated from the pia mater by subarachnoid space)
Subarachnoid space (fluid filled space containing CSF)
Pia mater - innermost later of the meninges and lies directly on the surface of the brain and spinal cord.
Brain
What are the 3 main types of brain haemorrhages? What causes them and where do they occur?
1) Subarachnoid haemorrhage (in the subarachnoid space) - due to Berry aneurysm rupture (circle of willis)
2) Subdural haemorrhage (in between the dura and arachnoid mater) - due to bridging vein rupture
3) Extradural haemorrhage (outside dura mater) - due to middle meningeal artery trauma
What makes up the anterior and posterior circulation of the brain?
Anterior - Internal carotid artery, anterior cerebral artery, middle cerebral artery
Posterior - Vertebral arteries, basilar artery, posterior cerebral arteries
Causes of Intracerebral haemorrhage
A hematoma is formed within the brain parenchyma.
RF- Hypertension, old males
Intracerebal haemorrhage causes:
- HYPERTENSION (basal ganglia, pons, cerebellum)
- Coagulopathy (patients on anticoagulants)
- Malignancy
- Trauma
(Symptoms same as stroke, investigation - NCCT) - immediate referral for neurosurgery assessment on confirmation of intracerebral haemorrhage
Subarachnoid haemorrhage
In addition to surgery, what would be given?
RF
Pathology
Symptoms
Investigations
Treatments
Bleeding in the subarachnoid space (where CSF is located - between the pia mater and arachnoid membrane), usually due to a ruptured cerebral aneurysm. (Blood pools in the basal cisterns)
RF- Hypertension, smoking, family history, autosomal dominant polycystic kidney disease. (45-70 YO black women)
Also associated with connective tissue disorders, sickle cell anaemia, drug use.
(High mortality and morbidity)
Berry aneurysm rupture
SYMPTOMS (TNM)
- Sudden occipital thunderclap headache (may occur during strenuous activity) - peaks within 1-5 mins and lasts more than an hour ————– Sentinal headaches can precede SAH by days/weeks
- Neck stiffness and meningism –> Kernig’s sign (pain on straightening knees when hips is flexed- Kan’t straighten knee) —- Brudzinski’s sign (reflex flexion of the patient’s hips and knees after elevation of the neck from supine position)
- Photophobia
- Nausea and Vomiting
- Neurological symptoms e.g. visual changes, dysphasia, reduced consciousness
- Seizures
INVESTIGATIONS
first line - Non contrast CT head (blood appears hyperdense in the subarachnoid space) - star shaped sign
If CT is positive - CT angiography can be used to locate the source of bleeding (after confirming the diagnosis)
If CT is negative or inconclusive, a lumbar puncture is performed after 12 hours of symptom onset –> may show xanthochromia (yellow CSF due to RBC haemolysis- bilirubin)
TREATMENT
1st line - Neurosurgery - endovascular coiling or neurosurgical clipping
and give Nimodipine - CCB
Subdural haemorrhage
RF
Pathology
Symptoms
Investigations
Treatments
Bleeding between the dura and arachnoid mater caused by a rupture of bridging veins in the outermost meningeal layer.
RF - Recent trauma, coagulopathy and anticoagulant use, >65 –> Elderlies and alcoholics
Can be caused by car crash, violent attack, (deceleration injuries, abused children- shaken baby syndrome)
SYMPTOMS (GILF)
Gradually onset - bleeding starts small and accumulates (can occur after days/weeks/months)
- Fluctuating Glasgow Coma Scale –> Diminished eye, verbal and motor response
- loss of bowel and bladder continence
- Increased intracranial pressure: Cushing’s triad –> widened pulse pressure, bradycardia and irregular respirations –> Papilledema
INVESTIGATIONS
Non contrast CT - crescent shape haematoma (can cross over suture lines)
Acute - Hyperdense (bright)
Subacute - isodense
Chronic (late) - hypodense (darker than the brain)
TREATMENT
- Surgery –> Craniotomy + burr hole (to relieve pressure due to high pressure)
What drug do you give to reduce intracranial pressure?
IV mannitol
Extradural haemorrhage
RF
Pathology
Symptoms
Investigations
Treatments
Bleeding between the skull and dura mater, usually caused by a rupture of the middle meningeal artery (in the temporoparietal region)
RF - young adults (as the more you age, the more firmly the dura is adhered to the skull), head trauma (70-90% of cases associated with skull fractures)
PATHOLOGY
Due to trauma to the head. (Rapidly expanding haematoma in contrast to subdural which is slowly expanding)
Mostly associated with a fracture of the temporal bone.
SYMPTOMS (a lot of it is due to compression) - LIND
- May have a lucid interval (temporary improvement in a patient’s condition after a traumatic brain injury, after which the condition rapidly deteriorates –> as the haematoma gets large enough to compress intracranial contents)
- Decreased GCS –> altered consciousness, confusion
- Nausea and vomiting
- Cushing’s triad –> widened pulse pressure, bradycardia and irregular respirations (increased intracranial pressure)
INVESTIGATIONS
Non contrast CT scan –> Lens shaped (bi convex) bleed that is limited by cranial sutures (points where skull bones join together) ,,, Midline shift
TREATMENT
Urgent surgery
(with ligation of the bleeding artery)
(IV mannitol to decrease ICP)
What is amaurosis fugax?
A possible symptom of TIA (or just a symptom in general) which describes a temporary monocular loss of vision which returns to normal afterwards –> due to a temporary occlusion of blood flow.
Very bad sign as it indicates that stroke is impending
What are the risk factors and common causes of Meningitis
Serious inflammation of the meninges
RF- Immunocompromised people, exposure to pathogens, crowding, extremes of age
PATHOLOGY
Main cause - Viruses (but less severe ) –> ENTEROVIRUSES (Coxsackieviruses), herpex simplex virus
Bacterial causes (less common but more severe) –> Mainly S.pneumonae and N.meningitidis
(Elderly can get listeria)
- Haemophilus influenzae type B can cause it also
Neonatal meningitis - Caused by group B strep and E.coli
N.meningitidis –>
- Gram negative diplococcus
- Presents with a non blanching rash
- MenACWY vaccine available
S.pneumoniae –>
- Gram positive diplococci in chains
- (Optochin sensitive)
- Pneumococcal conjugate vaccine
Group B strep –>
- Gram positive cocci in chains
- Main cause of neonatal meningitis (as it colonises the maternal vagina)
Listeria monocytogenes –>
- Gram positive bacillus found in cheese
- Mainly affects the extremes of age, (sometimes pregnant ladies)
Differentiate CSF samples between normal, bacterial and viral
Appearance
Normal - Clear fluid (gin coloured)
Bacteria - Cloudy/turbid
Virus - Clear fluid (gin coloured)
Cells
Normal - small number of lymphocytes
Bacterial –> increased neutrophilia
Virus –> Increased lymphocytosis
Protein
Normal –> 0.1 - 0.5 g/dl
Bacteria –> >1 g/dl
Virus –> <1g/dl - could still be mildly elevated
Glucose
Normal –> 66% of plasma glucose
Bacteria –> <50% of serum level
Virus –> normal
Encephalitis (briefly)
RF
Pathology
Symptoms
Investigations
Treatments
Viral infection of brain parenchyma
RF - Immunocompromised, extremes of age
PATHOLOGY
Caused by:
- HSV-1 –> 95% of cases
- CMV
- HIV
- EBV
SYMPTOMS
Confusion
Fever
Lethargy
Headache
Focal neurology (mostly the temporal lobe resulting in aphasia)
(If there are meningism symptoms, –> meningo-encephalitis)
INVESTIGATIONS
1st line - Lumbar puncture - CSF may show viremia with increased lymphocytes
MRI of head - possible temporal encephalitis
TREATMENT
Acyclovir - for HSV, VZV
(Gancyclovir for CMV)
Meningitis
Pathology
Symptoms
Investigations
Treatment
PATHOLOGY
For bacterial meningitis
- The bacteria reach the CNS either via haematogenous spread (More common) or direct extension from a contiguous site (invasion through the wall of an organ to other organs)
–> Once they enter the subarachnoid space, they multiply and lead to production of inflammatory mediators
SYMPTOMS
Meningism –> Headache, neck stiffness, photophobia (most important ones)
- Rash (only seen in N.meningitidis)
- Altered mental status
- Fever and vomiting
(however if it is due to viral infection e.g. HSV, patient may also present with encephalitis -> Treat with IV acyclovir)
INVESTIGATIONS
1st line –> Lumbar puncture and CSF analysis (CONTRAINDICATED IN SITUATIONS OF INCREASED INTRACRANIAL PRESSURE –> can lead to tentorial herniation
(CSF measurements - visual, culture, microscopy, protein, glucose)
- Blood culture + PCR
- Nose and throat swab (black charcoal and green viral)
- Stool PCR - for Enterovirus (as viral load is higher in stool than CSF)
TREATMENT
Primary care - IV benzylpenicillin STAT (while awaiting transfer to hospital) –> broad spectrum antibiotic
NOTIFY PUBLIC HEALTH ENGLAND
For - S.pneumoniae, N. meningitidis, Enterobacter, H.influenzae –> Ceftriaxone (3rd gen cephalosporin) + steroids (IV dexamethasone)
SO USUALLY CEFTRIAXONE FOR ANTIBIOTIC - DEXAMETHASONE GIVEN AFTER TO REDUCE ICP
Listeria –> Amoxicillin
Enterovirus - Nothing (self limiting)
Acyclovir - HSV, VZV
Multiple sclerosis
RF
Pathology
Symptoms
Investigations
Treatments
A chronic and progressive autoimmune condition involving the demyelination of the central nervous system (immune system attacks the myelin sheath of myelinated neurons) - Type 4 hypersensitivity
RF - 20-40 Females, family history, genetic factors- HLA-DR2
PATHOLOGY
Affects the oligodendrocytes of the CNS + causes inflammation and immune cell infiltration resulting in damage to myelin.
Characterised by multifocal areas of demyelination, loss of oligodendrocytes and astrogliosis (increase in astrocytes to try repair damage) and loss of axons.
Relapsing-remitting MS –> flare ups of the disease with periods of incomplete recovery in between. (most inflammatory activity)
Primary progressive MS –> Gradually worsening symptoms and an accumulation of disability (no relapses or remission) (least inflammatory activity)
Secondary progressive MS –> Form of the disease that develops from relapsing remitting MS
SYMPTOMS (remember first 5 mainly)
1) Charcot’s neurologic triad - Dysarthria, nystagmus, intention tremor
2) Optic neuritis: Blurred vision + painful eye movements (can’t see red properly) + internuclear ophthalmoplegia (inability to adduct eye)
3) Uhthoff’s phenomenon - temporary worsening of MS symptoms cause by heat
4) Paraesthesia
5) Lhermitte’s sign - electric shock sensation with neck flexion
Intention tremor, Incontinenece
Many other neurological symptoms: Ataxia, tremor, dysarthria, Horner syndrome - ptosis, miosis, anhidrosis
INVESTIGATION
First line and GS - MRI
Mcdonald criteria - 2 or more relapses disseminated in space and time (Space - MRI detecting lesions in another part of the CNS. Time - MRI showing evidence of new lesion since previous scan)
Others:
Can do a lumbar puncture which may detect IgG oligoclonal bands in the CSF - indicates inflammation and points toward MS.
TREATMENT
Acute (in episodes) –> IV methylprednisolone
Guillain Barre syndrome
- Symptoms and investigations
RF
Pathology
Symptoms
Investigations
Treatments
An AUTOIMMUNE acute paralytic polyneuropathy (affecting the peripheral nervous system)
RF- Preceding viral/Bacterial infection, HEV
PATHOLOGY
Causes an acute symmetrical ascending weakness (feet upwards) - may also cause sensory neuropathy
Usually triggered by infection: gastroenteritis, UTI
- Campylobacter jejuni (mostly)
- Cytomegalovirus
- EBV
Occurs due to molecular mimicry = Antibodies that match the antigens on pathogens (Campylobacter), also match that of the myelin sheath and axons –> causing damage and leading to symptoms
SYMPTOMS
- Symmetrical ascending weakness (starting at the feet and moving upwards)
- Hyporeflexia/areflexia (peripheral neuropathy) - difficulty holding objects, walking and standing up straight
- Respiratory distress (dyspnoea and shortness of breath)
- Peripheral loss of sensation
- Facial nerve weakness
INVESTIGATIONS
1st line - Nerve conduction studies (reduced conduction velocities)
- Lumbar puncture - elevated CSF protein and lymphocytes
- Spirometry to measure - VITAL CAPACITY
Can use Brighton criteria
TREATMENT
1st line - IV immunoglobulins - contraindicated in IgA deficiency (may result in anaphylaxis)
If IVIG is CI, Plasma exchange (to remove the antibodies)
+++++
Supportive treatment
e.g. Venous thrombosis prophylaxis - DOAC, LMWH
- Respiratory management - Intubation
Parkinson’s disease
RF
Pathology
Symptoms
Investigations
Treatments
A condition where there is a progressive reduction in dopamine in the basal ganglia (substantia nigra pars compacta)
RF - Increasing age, family history, (typically an older male)
PATHOLOGY
(Lewy bodies deposited in the substantia nigra)
Look at nigrostriatal pathway
There is a loss of nigrostriatal dopaminergic neurons in the substantia nigra pars compacta
But due to a loss of striatal dopaminergic output (within the basal ganglia) results in motor symptoms.
(May also precede the onset of lewy body dementia)
Symptoms (typically assymetrical)
- Resting tremor - tremor that is worse on one side and worse at rest –> pill rolling tremor
- Cogwheel rigidity - jerking in small increments upon passive flexion of the arm at the elbow
- Bradykinesia (slower and smaller movements)
- Postural instability - increasing risk of falls
- Micrographia - handwriting gets smaller
- Shuffling gait
- Hypomimia - reduced facial movements and facial expression
- Anosmia - loss of smell
- Constipation
INVESTIGATIONS
Clinical diagnosis
Bradykinesia + 1 of the following
- Muscle rigidity
- Resting tremor
- Postural instability
(UK Parkinson’s disease society brain bank clinical diagnosis criteria)
TREATMENT
(No cure, treatment focused on controlling symptoms and minimising side effects)
1st line - Levodopa
(Carbidopa usually prescribed with levodopa)
Can consider a COMT inhibitor (Entacapone which prevent peripheral degradation of levodopa, allowing a higher concentration to cross the BBB)
(Patient may experience ‘on-off’ fluctuations –> well controlled period with sudden decline after)
Huntington’s disease (chorea)
RF
Pathology
Symptoms
Investigations
Treatments
An autosomal dominant genetic condition that causes progressive neurological dysfunction
PATHOLOGY
A trinucleotide (CAG) repeat disorder involving a genetic mutation in the HTT gene on chromosome 4 (codes for huntingtin protein -)
<35 repeats - no huntington’s
35-55 - huntington’s
>60 severe huntington’s
(huntingtin deposited in the striatum)
It displays genetic anticipation –> a feature where successive generations have more repeats in the gene resulting in earlier age of onset and increased severity of disease.
SYMPTOMS
Chorea - involuntary, random, irregular abnormal body movements
Psychiatric changes - Irritability (or some kind of personality change- gambling, unusual purchase)
Depression
INVESTIGATIONS
Clinical diagnosis
Family history of earlier and more severe Huntington’s
GS - Genetic test (CAG repeat test) –> a positive result is more than 35 CAG repeats on chromosome 4
TREATMENTS
1st line - counselling for patient and family
Tetrabenazine for chorea
(Antidepressants for depression)
What is dementia? What are the types of dementia?
A neurodegenerative disorder resulting in decreased cognition including memory, judgement and language over time
Alzheimer’s
Lewy body
Frontotemporal
Vascular
Alzheimer’s
RF
Pathology
Symptoms
Investigations
Treatments
A chronic neurodegenerative disease with a slow but progressive decline. (most common type of dementia)
RF - Advanced age, family history, genetics (ApoE-4), down’s syndrome
PATHOLOGY
Associated with ApoE-4 allele (in familial Alzheimer’s, late onset)
Associated with Down’s (Increased expression of APP, increasing amount of amyloid plaque build up, earlier onset)
Excess interneuronal amyloid peptides due to an overproduction or diminished clearance of beta amyloid (breakdown product of amyloid precursor protein) results in formation of plaques which can cause inflammatory processes to occur resulting in synaptic and neuritic injury and cell death. This disrupts signalling resulting in impaired brain function. (memory)
Aggregation of abnormally phosphorylated tau protein (that stabilises microtubules in the cell) accumulates into neurofibrillary tangles
Essentially
1) Plaques are made up of beta amyloid and are extracellular
2) Neurofibrillary tangles are intracellular and composed of hyperphosphorylated tau
SYMPTOMS (Steady progressive decline over time)
- Memory loss
- Agnosia - can’t recognise things/people
- Apraxia - can’t do basic motor skills
- Aphasia - can’t talk as well as normal
- Disorientated and confused
Investigations
Use mini mental state examination (MMSE) – <25=dementia or memory impairment screen (MIS)
(Might want to arrange blood tests to exclude reversible causes of cognitive decline e.g. ESR, CRP, U and E, calcium, B12, folate HbA1C)
GS - Brain MRI may show cortical atrophy
TREATMENT
Supportive - specialist dementia nurse+ acetylcholinesterase inhibitor - DONEPEZIL
(increases the amount of acertylcholine to improve communication between neurons –> slowing down disease progression.
Lewy body dementia
-Symptoms
Pathology
Symptoms
Investigations
Treatments
PATHOLOGY
Spherical lewy body proteins (composed of alpha synuclein + ubiquitin) accumulate in the cortex (associated with parkinsons disease)
SYMPTOMS
- Visual hallucinations
- Parkinsonism features - bradykinesia, rest tremor, rigidity
- Fluctuations in cognitive ability - cognition, attention and arousal
- Constipation
- Anxiety and depression
- Sleep disorders
INVESTIGATIONS
Use mini mental state examination (MMSE) <25 =dementia or memory impairment screen (MIS)
(Might want to arrange blood tests to exclude reversible causes of cognitive decline e.g. ESR, CRP, U and E, calcium, HbA1C)
GS - Brain MRI may show cortical atrophy
TREATMENTS
Supportive care (multifactorial interventions to increase physical therapy, occupational therapy, a social worker should be made available + acetylcholinesterase inhibitor (DONEPEZIL)
Frontotemporal dementia (pick’s disease)
RF
Pathology
Symptoms
Investigations
Treatments
PATHOLOGY
- Autosomal dominant - chromosome 17
- RF - family history of MND
Neuron damage and death occur in the frontal and temporal lobes due to deposition of tau protein within the lobes. (most cases)
SYMPTOMS
If temporal more affected - Speech and language disorders (speech takes effort and is not fluent, progressive decline in the understanding of word meanings)
If frontal more affected - thinking and memory disorders (altered emotional responsiveness, impulsivity,
INVESTIGATIONS
MMSE - mini mental state examination
Brain MRI - focal atrophy in the frontal and/or temporal lobes
TREATMENT
Supportive care
(if irritable, restless, agitation, agressive) - LORAZEPAM (benzodiazepine)
Vascular dementia
RF
Pathology
Symptoms
Investigations
Treatments
A chronic progressive disease of the brain resulting in cognitive impairment.
RF - >60 years, obesity, hypertension, smoking
PATHOLOGY
2nd most common dementia
It is progressive in a stepwise fashion - period of stability at one level of functioning before a decline progression followed by another period of stability
Mostly due to cerebrovascular infarcts that commonly affect white matter of the cerebral hemispheres. Can be a result of embolisation, thrombosis, lacunar infarction, hypoxia, ischaemia –> essentially strokes and TIA.
SYMPTOMS
(Most likely has a history of strokes)
- Cognitive impairment (difficulty solving problems, apathy, poor attention, mood disorders)
- Presence of focal upper motor neuron signs (hemiparesis, dysarthria and dysphagia)
INVESTIGATIONS
MMSE - mini mental state examination
MRI of brain - cerebrovascular lesion (if MRI CI, CT scan)
TREATMENT
Antihypertensive - Ace inhibitors (ramipril)
Examples of primary and secondary headaches
Primary - Cluster, migraine, tension
Secondary (due to underlying condition) - Giant cell arteritis, infection, trauma, cerebrovascular pathology
