Neurology Flashcards
What is a good surgical sieve for neurological lesions?
VINDIE
Vascular Inflammation Neoplastic Degenerative Infective Episodic
Neurology symptoms - sudden tempo causes
= vascular/trauma/epilepsy/migraine
Neurology symptoms - hours/days tempo causes
= inflammation/infection
Neurology symptoms - days/weeks tempo causes
= inflammation/rapid mass lesions
Neurology symptoms - months tempo causes
= slower mass lesions
Neurology symptoms - years tempo causes
= degenerative
Neurology symptoms - since early life
= congenital (can evolve as child grows)
Headache history
Age Location of Pain Pattern of pain Tempo – important for diagnosing cause! Associated Symptoms
What can cause blackouts/LOC?
what is important to establish from the Hx?
epileptic seizures,
fainting attacks,
psychological causes (dissociation),
cardiac causes.
What were they doing before, during, and after?
What is the spinothalamic tract for?
Where do its fibres cross?
sensation of pain and temperature.
Crosses near where it enters the spinal cord
UMN and LMN origins
UMNs start in the primary motor cortex, within the cerebral hemispheres.
In the medulla this decussates to the other side of the spinal cord (=> corticospinal tract).
This synapses on the anterior horn cell of the spinal cord to a LMN
The LMN synapses on the muscle.
Signs and Symptoms in UMN lesions
secondary changes in excitability
Hypertonia, Hyperreflexia, Babinski +ve (extensor plantar), Clonus, weakness
UMN signs can take days to weeks to develop – Pt can be HYPOreflexic in this time.
Signs and Symptoms in LMN lesions
shows effects of loss of nerve input to muscle
Hypotonia, Hyporeflexia, Wasting, Fasciculations, weakness
Where is weakness worse in UMN lesions?
Extensors of the arm – shoulder abduction, triceps, wrist and finger extensors.
Flexors of the leg – hip flexion, knee flexion, ankle dorsiflexion
(flexors of the arm and extensors of the leg may become stronger to compensate)
What signs and symptoms would you expect with a lesion in the cerebral hemisphere?
Contralateral Hemiplegia – arm and leg
Contralateral Motor and sensory signs
UMN signs
May have cognitive signs depending on where the lesion is.
=> Aphasia (L)
=> Spatial neglect (R).
Weakness will SPARE the forehead.
What signs and symptoms would you expect with a lesion in the brainstem?
Abnormal eye movements
Vertigo
UMN contralateral or bilateral weakness
Cranial nerve signs and symptoms
+/- Crossed sensory signs
+/- Weakness of face, swallowing and speech
+/- Cerebellar signs
+/- Horners’ sign
symptoms of cerebellar ataxia?
impaired coordination in the torso or arms and legs.
frequent stumbling.
an unsteady gait.
uncontrolled or repetitive eye movements.
trouble eating and performing other fine motor tasks.
slurred speech/vocal changes.
What is Horner’s Sign?
Why does it occur?
Constricted pupil (miosis),
Drooping of the upper eyelid (ptosis),
Absence of sweating of the face (anhidrosis),
“Sinking” of the eyeball (enophthalmos).
Occurs when there is damage to the sympathetic trunk
What signs and symptoms would you expect with a lesion in the spinal cord?
There will be UMN weakness unless the lesion is at the cauda equina.
Typically bilateral weakness, motor and sensory loss.
=> Lesion in thoracic spinal cord – affects legs
=>Lesion in cervical spinal cord – affects arms and legs.
Sensory loss will lead to a “sensory level” above which there is feeling, and below which there isn’t.
Joint position sense, light touch and pain/temp may be differently affected
Where do light touch and joint position sense travel in the spinal cord?
dorsal columns
Where do Pain and temperature sense travel in the spinal cord?
spinothalamic columns
where does the spinal cord end?
what would a lesion below this additionally effect?
L1
typically affect the sphincters, function can be permanently lost.
What signs and symptoms would you expect with a lesion in the root nerve?
LMN weakness
Sensory loss
Relevant reflex lost
The pattern of affected muscles and sensory loss is crucial – root or individual nerve distribution?
Anterior horn cell disease (motor neurone disease) will not have sensory loss and may have mixed UMN and LMN signs.
What signs and symptoms would you expect in muscle disease?
Proximal weakness is a common pattern – shoulder/thigh muscles.
Neck and respiratory weakness
Eye muscle or swallowing weakness
Muscle that fatigues (weaker with repetitive movement) seen in myasthenia gravis.
What components do you examine in a PNS exam of the limbs?
Inspection Tone Power Reflexes Coordination and function Sensation
What visual defect would an ipsilateral optic nerve lesion cause?
monocular loss of vision
What visual defect would an optic chiasm lesion lesion cause?
bitemporal hemianopia
What visual defect would a contralateral optic tract lesion cause?
Homonymous hemianopia
What visual defect would a contralateral optic radiation lesion cause?
Homonymous quadrantanopia
What visual defect would a visual cortex lesion cause?
Macular sparing in homonymous hemianopia (or quadrantanopia)
What might a trigeminal nerve lesion cause?
Wonky/weak jaw
Wasted muscles of jaw
Numb face
Clinical presentation of SAH
“Thunderclap” headache
=> develops over seconds, extremely intense, often occipital
Vomiting (after headache begins)
Photophobia
Increasing drowsiness/coma
Focal signs
Neck stiffness
Positive Kernig’s sign – takes 6 hours to develop
Papilloedema – may be present, along with retinal haemorrhages
Why can there be photophobia in SAH?
blood can irritate the meninges, causing signs of meningism
aseptic meningitis
Kernig’s Sign
Flexion of thighs at the hip, and the knees at 90 degree angles
Assess whether subsequent extension of the knee is painful (leading to resistance)
Resistance leads to positive Kernig’s Sign
When and how can SAH present atypically?
particularly in the elderly,
with seizures, confusion or mild headache
What are the causes of SAH?
- Trauma
- Spontaneous:
- Berry aneurysm
- Arterio-venous malformation
- Cryptogenic
Which conditions/factors which can predispose someone to SAH?
Marfan’s and Ehler’s Danlos Syndrome
Polycystic kidney disease
Smoking and ETOH
Where do Berry Aneurysms most commonly develop?
Anterior communicating artery – most common
Posterior communicating artery
Middle cerebral artery
risk factors for berry aneurysm
More common in PCKD
FHx, smoking, HTN, connective tissue disorders
AV Malformation
Congenital collection of abnormal arteries/veins
Have a tendency to re-bleed if symptomatic once
A cause of SAH and also sometimes epilepsy
Complications of SAH
Death (30% die immediately)
Rebleed (3-4 days for aneurysm, years for AVM)
Hydrocephalus - fibrosis in CSF pathways
Cerebral vasospasm
Subdural haematoma
= a collection of blood in the subdural space following the rupture of a vein.
Acute SDH Presentation
Within 72 hours.
Occurs in severe acceleration-deceleration head injury, often with co-existing brain damage.
LOC, low GCS, anisocoria, motor deficit
May be a lucid interval
What is a Lucid interval in SDH?
The patient can appear relatively well and normal for a few hours after the injury, but subsequently deteriorates and LoC as the haematoma forms
How will acute SDH appear on CT?
appear hyperdense on CT – classic cresenteric shape of white density
Sub-acute SDH Presentation
May occur spontaneously, or after minor trauma
Signs and symptoms of raised ICP being to develop ~2 weeks after the insult or start of the bleed, and are often more subtle/fluctuant
what are risk factors for sub-acute SDH?
The elderly – cerebral atrophy and increased venous fragility
Alcohol abuse – clotting is reduced
Seizures
Anti-coagulants and coagulopathies
How can sub-acute SDH appear on CT?
blood may be isodense or hypodense to the brain parenchyma
What are some signs of raised ICP?
Headache Drowsiness Confusion Focal neurological signs Eventually stupor and coma occur.
Complications of SDH
Death
Raised ICP
Cerebral oedema.
Recurrent haematoma formation during recovery.
Seizures.
Wound infection, subdural empyema, meningitis.
Permanent neurological or cognitive deficit due to pressure effects on the brain.
Coma/persistent vegetative state.
What is a stroke?
= an acute, focal neurological deficit of cerebrovascular origin that persists >24 hours
What is a TIA?
= an acute, focal neurological deficit of cerebrovascular origin that persists <1 hour, without signs of cerebral infarction on MRI scanning.
very high risk of stroke within 4 weeks of TIA
What is Amaurosis Faugax ?
= sudden, transient loss of vision in one eye.
occurs in TIA of the retina
Can also occur due to ocular disease or migraine
What are the types of stroke?
- ~85% ischaemic
2. ~15% haemorrhagic.
Causes of ischaemic stroke
Arterial embolus from a distant site
Arterial thrombosis in atheromatous carotid/vertebral/basilar artery
Systemic hypoperfusion (general circulatory problem)
Causes of haemorrhagic stroke
Sub-arachnoid haemorrhage
Intra-cerebral haemorrhage
Risk factors for Ischaemic Stroke
NON-MODIFIABLE Age Male sex Family History Hypercoagulable states Non-white ethnicity AF
MODIFIABLE: Hypertension Hypercholesterolaemia Diabetes Smoking Alcohol Poor diet Low exercise Increased weight Use of oestrogen-containing oral contraceptives
Risk factors for Haemorrhagic Stroke
Family History
Uncontrolled HTN
Vascular abnormalities (aneurysms, AVMs, HHT)
Coagulopathies/anticoagulant therapies
Heavy recent alcohol intake.
Illicit drug use (mostly amphetamines and cocaine)
Trauma
What are the clinical features of a stroke?
typical of hemispheric lesion:
Facial weakness – sparing forehead.
Contralateral limb weakness/hemiplegia and loss of sensation.
Higher Dysfunction
What are forms of Higher Dysfunction?
Expressive aphasia
Receptive aphasia
Apraxia
Asterognosis
Agnosis
Inattention (neglect)
Apraxia
difficulty in performing task, despite intact motor function.
Asterognosis
inability to identify objects in both hands, despite intact sensation.
Agnosis
inability to recognise objects/people/sounds/smells despite the specific sense intact and no memory loss.
Inattention (neglect)
inability to attend to stimuli despite intact senses.
Expressive aphasia
inability to express language despite intact comprehension
Receptive aphasia
inability to understand commands, may have fluent but meaningless speech
What investigation is required for suspected stroke?
urgent CT - identify if ischaemic or haemorrhagic
Total Anterior Circulation Syndrome (TACS)
= proximal MCA occlusion
Affecting the areas of the brain supplied by both the middle and anterior cerebral arteries
All three of:
- Higher dysfunction (incl. decreased level of consciousness)
- Homonymous hemianopia
- Contralateral hemiplegia and/or sensory loss (>2 of face, arm, leg)
Partial Anterior Circulation Syndrome (PACS)
= distal MCA or ACA occlusion
A less severe form of TACS, in which only part of the anterior circulation has been compromised.
Requires 2 of the 3 TACS criteria.
Lacunar Stroke (LACS)
= occlusion of lacunar branch of MCA
A subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions.
One of the following:
- Pure motor symptoms
- Pure sensory symptoms
- Pure sensorimotor symptoms
- Ataxic hemiparesis
Posterior Circulation Stroke (POCS)
= PCA occlusion.
There will be damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum, thalamus, and brainstem).
Presents as:
- Cranial nerve palsy AND contralateral motor/sensory deficit.
- Conjugate eye movement problems (e.g. nystagmus, double vision)
- Cerebellar dysfunction
- Isolated homonymous hemianopia
What are complications of a stroke?
Cognitive impairment
MI, Heart failure
Dysphagia
Aspiration pneumonia
UTI
DVT, PE
Dehydration, malnutrition
Pressure sores
Depression
Orthopaedic complications and contractures
What is the association of AF with stroke?
The left atrial appendage is the usual site of thrombus formation in AF.
Stasis of blood leads to formation of a thrombus.
Thrombus can embolise to the posterior/anterior cerebral circulation, causing embolic stroke.
what is meningism?
= meningeal irritation
Symptoms and signs of meningism
- Global headache
- Neck and back stiffness
- Nausea and vomiting
- Photophobia
Signs:
- Nuchal rigidity – neck resists flexion.
- Brudzinski sign – flexion of the neck results in hip flexion
- Kernig’s sign – knee extension elicits pain and resistance to further extension.
what is Brudzinski’s sign?
positive when flexion of the neck results in hip flexion
what is Kernig’s sign?
positive when knee extension elicits pain and resistance to further extension
what is meningitis?
= inflammation of the meninges.
What are the routes of infection to the meninges?
- Blood-borne
- Para-meningeal suppuration - e.g. otitis media, sinusitis
- Direct spread through a defect in the dura - e.g. post-surgery, trauma
- Direct spread through the cribriform plate (rare)
What is a sign of a defect in the dura?
CSF leaking out of the nose/ear is a sign of a defect in the dura
Complications of meningitis
- Death
- Subdural collection of pus
- Cerebral vein thrombosis
- Hydrocephalus
• 9-15% deafness - particularly in children, associated with Hib infection
- Convulsions
- Visual/motor/sensory deficit
How can meningitis cause hydrocephalus?
subsequent scarring can alter CSF absorption, accumulation of CSF can cause expansion of ventricles
What are the common bacterial causes of meningitis?
What age groups are affected?
Neisseria meningitidis - Children, Young adults
Streptococcus pneumoniae - Elderly, Children <2 years
(Haemophilus influenzae type B, Hib) - Children <5 years
Escherichia coli - Neonates
Listeria monocytogenes - Neonates, Immunocompromised
Streptococcus agalactiae (Group B Strep) -Neonates
What are the viral causes of meningitis?
Enterovirus, HSV, VZV, EBV, Mumps.
Clinical features of meningitis
Classic clinical triad = headache, fever and neck stiffness
- Global headache
- Neck and back stiffness
- Nausea and vomiting
- Photophobia
Others:
- Seizures
- Focal neurological symptoms
- Lethargy and confusion
- Stupor and Coma
when can meningitis present atypically?
may be observed in the very young, very old or immunocompromised
Neurological signs of meningitis
- Impaired conscious level
- Cranial nerve palsies – due to RICP or direct damage (principally 3,4,6 or 7)
- Focal or generalised seizures
- Papilloedema and other signs of RICP
- Focal neurological signs – e.g. hemiparesis, dysphasia, hemianopia due to ischaemia from vascular inflammation (arteritis or venous thrombophlebitis)
- Sensorineural deafness
Systemic signs of meningitis
- Pyrexia
- Extracranial infection (e.g. sinusitis, otitis media, mastoiditis, pneumonia)
- Arthritis (N. meningitidis)
- Endocarditis
- Skin – Non-blanching petechial/purpuric rash (suggesting meningocococcaemia)
- Endotoxic shock
Investigation of meningitis - bedside tests
FBC, U&E, LFT, CRP, Clotting, Blood cultures
Meningococcal/pneumococcal PCR
Lactate, Glucose
Throat swab
?Stool sample
?HIV
Investigation of meningitis - imaging/invasive
CT, MRI (do not delay LP unless signs of raised ICP)
LP (if possible)
=> Opening Pressure
=> CSF – Protein, cell count, MCS, glucose (+serum glucose), vPCR
what are signs of raised ICP that may mean a lumbar puncture is contraindicated?
- GCS <12
- Seizures
- Focal neurological signs
• Papilloedema (can be slow in its development and lack of papilloedema does not rule out raised ICP)
what are some other contraindications for lumbar puncture (other than raised ICP)
Signs of meningococcal septicaemia
Evidence of potential bleeding risk (platelets <50, INR >1.2)
History of clotting disorder
CSF composition - bacterial meningitis
Extremely elevated leucocytes
=> mainly neutrophils
raised protein
low glucose
CSF composition - viral meningitis
elevated leucocytes
=> mainly lymphocytes (unless early presentation)
slightly raised protein
normal glucose
CSF composition - TB meningitis
elevated leucocytes
=> mainly lymphocytes (unless early presentation)
very raised protein
very low glucose
What glucose level in the CSF is normal?
60-80% of serum levels.
How is meningitis managed?
- Antibiotics
- Adequate oxygenation
- Prevention of hypoglycaemia and hyponatraemia
- Anticonvulsants – if patient is fitting
- Decrease ICP – prevent brain herniation
Viral encephalitis - clinical features
Fever Seizures Altered mental state Headache Focal neurological deficit
How is viral encephalitis investigated?
in the same way as meningitis
How is viral encephalitis managed?
IV aciclovir (oral not acceptable) Aggressive management of seizures
Even if the LP picture does not add up to viral encephalitis, if there is enough clinical suspicion then you should treat with IV acyclovir
Cerebral abscess - clinical presentation
Presentation will depend on the location of the abscess
- Focal neurological signs
- Raised ICP
- Headache 70-95% (short duration)
- Fever variable
- CRP and ESR raised
• (CSF pleocytosis - if done before suspicion of brain abscess – contraindicated to do lumbar puncture if raised ICP is suspected))
CNS infections in the immunocompromised
More susceptible to less common organisms
They may not respond to usual meningitis treatment
Dysdiadochokinesis
= the inability to execute rapidly alternating movements, particularly of the limbs
e.g. demonstrated by asking the patient to pronate and supinate an arm at speed
What signs can lesions of the cerebellum cause?
Dysdiadochokinesis Ataxia Nystagmus Intension Tremor Slurred Speech Hypotonia
CT vs MRI in neurology
CT is preferred in the acute setting - intracranial haemorrhage and (broadly) tumours and abscesses
MRI superior in detecting most other things.
How does a subarachnoid haemorrhage normally present on CT?
hyperdensity within the sulci of the brain
How does a parenchymal haemorrhage normally present on CT
a focal area of hyperdensity, sometimes surrounded by an area of low density, which is parenchyma oedema.
what are the two types of cerebral parenchymal oedema?
- Vasogenic oedema:
• Normally associated with tumour
• Involves white matter, spares cortex. - Cytotoxic oedema:
• Oedema is diffuse and involves both the grey and white matter.
• Tends to be seen in strokes.
