Neuro 4 Flashcards
Why does raised ICP matter?
cerebral perfusion pressure (CPP) has relationship with cerebral blood flow (CBF)
>not linear
>termed autoregulation
late reflex brainstem ischaemia in raised ICP (intracranial pressure)
>will result in increased MAP to ensure CPP is maintained (Cushing reflex)
What happens when CPP is more than 150 mg Hg?
loss of control of blood flow – ischaemic forced vasodilation
Lisa brain swelling (brain oedema) – ICP = MAP – thus no blood flow
What happens when CPP is less than 50mmHG?
cannot perfuse brain adequately with oxygen and nutrients,
>leads to loss of function
What can cause raised ICP?
information – meningitis, encephalitis, abscess
vascular causes – intracranial haemorrhage (natural disease or traumatic), brain swelling (traumatic brain injury, physical, or physiological (cardiac arrest))
tumours
hydrocephalus
What are the types of brain herniation?
Cingulate Central Uncal Cerebrotonsullar Upward Transcalvarial
How are the clinical signs of raised ICP explained by their pathology?
Glasgow coma scale – reason cortex and brainstem
pupillary dilation – squeezing stretch on cranial nerve 3
localising signs – squeeze on decussation of Corsical spinal tracks and posterior columns
Where are the common sights of brain tumours?
In adults, mostly above tentorium
In children most are below (and mostly primary)
What is ischaemic penumbra?
Tumours occupy space and therefore squeeze nearby tissue and cause local ischaemia
lead to loss of function around it,
>Removal of oedema around tumour improves function
can salvage in tumours and head injury
What is glioma (astrocytoma)
tumours resembling cells of astrocytes differentiation
CMS supporting cells with diffuse areas (not encapsulated)
>do not metastasise outside the CNS
Often young adults
What is the prognosis of glioma?
grades of differentiation predict prognosis
high-grade has worst outlook Outlook
>grows rapidly and responds poorly to surgery – median survival 36 weeks
site important outcome regardless of grade
low-grade (cystic) grows very slowly
What is medullary blastoma
the tumour of the primitive neural ectoderm – small blue round cell tumour
children especially but not exclusively
posterior fossa especially brainstem affected
poor outcome because of central site and difficult access for surgery
What is meningioma
tumour of the Arapahoe sites – those that make up coverings of the brain 2nd most common type it is a connective tissue tumour often benign do not metastasise can be locally aggressive can invade the skull
What is a nerve sheath tumour?
Around nerves in the CNS or PNS
acoustic neuroma is most common
found near CN VII can results in unilateral deafness
found in posterior fossa, often benign lesion removal to technically difficult and can cause collateral cranial nerve injury as cranial nerve VII is very close
What is a Benign tumour of the posterior pituitary in the pituitary fossa?
often secrete pituitary hormone
many non-functional squeeze normal gland stops working – panhypopituitarism
hormone secreted reflected on clinical signs (Growth hormone result in acromegaly or giantism)
grow superiorly and impinge on optic chiasma– visual signs depending on exact site
What is CNS lymphoma
high grade neoplasm, usually diffuse large B cell lymphoma
often deep in central site therefore difficult to biopsy
difficult to treat as drugs do not cross blood-brain barrier
generally do not spread outside CNS
What is capillary heamanglioblastoma?
Space occupying tumour that may bleed
most often in the cerebellar hemispheres
What are secondary tumours?
mostly carcinomas of common tumours
present with focal signs usually
some can be removed surgically although the site matters
tend to be encapsulated and surrounded by oedema
histology of the primary tumour
What are the most common tumours that metastasise to the brain?
Lung
Breast
Kidney
GI
What are the clinical features of a brain tumour?
Cerebral oedema Increased intracranial pressure Focal neurologic deficits Obstruction of flow of CSF Pituitary dysfunction Papilledema (if swelling around optic disk
What are the specific clinical features of a cerebral tumour?
Headache Vomiting unrelated to food intake Changes in visual fields and acuity Hemiparesis or hemiplegia Hypokinesia Decreased tactile discrimination Seizures Changes in personality or behaviour
What are the specific clinical features of a brainstem tumour?
Hearing loss (acoustic neuroma) Facial pain and weakness Dysphagia, decreased gag reflex Nystagmus Hoarseness Ataxia (loss of muscle coordination) and dysarthria (speech muscle disorder) (cerebellar tumours)
What can cause small pupils?
old age Bright light Miotic eyedrops opiate overdose Horner's syndrome
How do you diagnose a brain tumour?
CT
MRI
MRI angiography
PR spectroscopy
What are the clinical features of a frontal lobe tumour?
Inappropriate behavior Personality changes Inability to concentrate Impaired judgment Memory loss Headache Expressive aphasia Motor dysfunctions
What are the clinical features of a parietal lobe tumour?
Sensory deficits Paresthesia Loss of 2 pt discrimination Visual field deficits Temporal lobe Psychomotor seizures – temporal lobe-judgment, behavior, hallucinations, visceral symptoms, no convulsions, but loss of consciousness Occipital lobe Visual disturbances
What are the types of intraaxial tumours?
Gliomas Astrocytoma (Grades I & II) Anaplastic Astrocytoma(III) Glioblastoma Multiforme(IV) Oligodendroglioma Ependymomas Medulloblastoma CNS Lymphoma
What do intraaxial gliomas originate from?
Intra-axial gliomas originate from glial cells; they affect brain by invasion and infiltration.
What are the types of extraaxial tumours?
Meningioma Metastatic Acoustic neuromas (Schwannoma) Pituitary adenoma Neurofibroma
Where do extraaxial tumours orginate?
From supporting structures of CNS
How does astrocytoma present?
seizures,
headache,
slowly progressive neurological deficits
What are oligodendrogliomas?
normally about 40 years old
distinguish pathologically from astrocytoma’s by the characteristic fried egg appearance
rises from Myelin
found in frontal lobe superficially
presents with seizures, headache, slowly progressive neurological deficits
What are glioblastomas?
most common primary brain tumour in adults
presents 40 to 60 years old more common in males
has poor prognosis and can look like a butterfly lesion
tumour infiltrates a long white matter tracts and can cross corpus callosum
may arise de novo or evolve from a low grade glioma
How do glioblastomas present?
presents procedures headache and slowly progressive neurological deficits
Where are glioblastomas found?
found in frontal and temporal lobes, or basal ganglia
What is the venous drainage of the brain?
veins do not accompany arteries, large venous sinuses within dura
Fed by bridging veins from brain – cross meninges brain to skull
emissary veins into veins outside skull
What is a stroke?
focal neurological deficit – loss of function affecting specific region of central nervous system due to disruption of blood supply
causes damage to brain tissue due to lack of oxygen and nutrients
most strokes due to thrombi and pulled ischaemic strokes
one in 10 caused by ruptured blood vessels or haemorrhagic strokes
What are the key features of a stroke?
focal neurological deficit
sudden weakness or numbness – face, arm or leg, most often one side of body
others
confusion, difficulty speaking or understanding speech
difficulty seeing one or both eyes
difficulty walking, dizziness, balance coordination loss
severe headache with no known cause
unconsciousness
clinical presentation gives indication to possible anatomy of lesion
What are the different types of stroke?
transit ischaemic attack (TIA) – less than 24 hours
minor stroke – growth in 24 hours but minor neurological deficit
disabling stroke – growth in 24 hours with persistent disability that impairs independence
can occur in either carotid or Priscilla are free territory
What is the pathogenesis of ischaemic stroke?
brain very sensitive to oxygen ischaemia
cerebral blood flow takes about 15% of cardiac output
a few minutes of hypoxaemia or anoxia will cause brain ischaemia
can lead to infarction, damage to neurons is permanent, they do not regenerate
roughly 85% of strokes have potential for thrombolysis
What are the causes of ischaemia?
atherosclerosis
thrombosis
embolism
hypertension – cardiac arrest, massive blood loss
arterial spasm following Symptomatic treatment haemorrhage
Systemic vascular disease e.g. arthritis
mechanical compression – head injury causing brain swelling, spinal cord compression
venous obstruction – dual vein thrombosis, mediastinal tumour
What are the sources of thrombolysis and emboli?
thrombotic causes – arteriosclerosis, smoking, diabetes
Emboli sources – cardiac arrhythmia, thoracic aortic aneurysm
distribution, thrombi, single large infarct
Emboli distribution – multiple smaller infarcts
What is watershed?
internal pattern of ischaemia and infarction due to periphery of perfusion territory of major arteries affected
What is the mechanism of global ischaemia?
systemic hypertension and local atherosclerosis
lead to decreased flow, and therefore decrease oxygen
neurons in superficial cortex, hippocampus, thalamus, cerebellum are most sensitive
What is the histology of infarcts?
loss of neurons causes clinical functional deficits
foamy macrophages – part of repair process, leads to gliosis
Gliosis CNS equivalent or fibrosis
What is the pathogenesis of haemorrhagic stroke?
roughly 15% of strokes
intracerebral haemorrhage – associated with systemic hypertension over 50s, 80% in basal ganglia, brainstem cerebellum, cerebral cortex
lovely growing intracranial space occupying lesion an increase in intracranial pressure
What can cause a subarrachnoid haemorrhage?
Rupture of secular (Berry) aneurysm on the circle of Willis
>branching point on the interior part circle of Willis
internal carotid, anterior communicating artery and middle cerebral artery
most are less than 10 mm but up to 56 mm seen
Can contain thrombus so imaging can underestimate true size
What is optic neuritis?
demyelination within the optic nerve monocular visual loss pain on eye movement reduced visual acuity reduced colour vision optic disc may be swollen often associated with multiple sclerosis
What are the disorders of eye movement?
isolated 3rd, 4th, 6th nerve palsy
combination of above
supra-nuclear gaze palsy
nystagmus
What is 3rd nerve palsy?
microvascular – diabetes, hypertension
painless, people spared
compressive – posterior communicating artery aneurysm, raised ICP
painful pupil affected
What can cause 6th nerve palsy?
numerous causes including idiopathic diabetes meningitis raised ICP
What can cause nystagmus?
can be congenital serious visual impairment peripheral vestibular problem Central vestibular/brainstem disease cerebellar disease toxins
What can cause trigeminal neuralgia?
Paroxysmal attacks of lancinating pain Triggers Middle age and older Caused by vascular loop Compression fifth nerve in the posterior fossa Treated medically with carbamazepine Surgical options if medication resistant
What is Bell’s palsy?
Unilateral facial weakness Lower motor neurone type Often preceded by pain behind ear Eye closure affected Risk of corneal damage Treated with steroids Usually good recovery
What is pseudobulbar palsy?
Bilateral UMN lesions
>e.g. in vascular lesions of both internal capsules, MND
What are the symptoms of pseudobulbar palsy?
- dysarthria
- dysphonia
- dysphagia
- spastic, immobile tongue
- brisk jaw jerk
- brisk gag reflex
What is bulbar palsy?
Bilateral LMN lesions affecting IX - XII
eg. MND, polio, tumours, vascular lesions of the medulla and syphilis
What are the symptoms of bulbar palsy?
- wasted, fasciculating tongue
- dysarthria
- dysphonia
- dysphagia
Be careful when feeding because of these
What is a coma?
State of unreliable psychological responsiveness
>in which subject lies with eyes closed
>and shows no psychological understandable response to external stimulus
What does conciousness depend on?
Intel is sending reticular activating system – is alert and awaking element of consciousness
functioning cerebral cortex of both hemispheres determines content of that consciousness
What is persistent vegative state?
state which brainstem recovers to a considerable extent but there is no evidence of cortical function
arousal wakefulness but patient does not regain awareness purposeful behaviour of any kind
What is locked-in syndrome?
total paralysis below level IIIrd nerve nuclei
able to open elevate and press eyes but no horizontal eye movements nor other voluntary eye movement
What are the neurological assessments of coma?
GCS
brainstem function
motor function plus reflexes
What cranial nerves cause abnormal pupillary reactions?
II - optic
III - oculomotor
What cranial nerves cause abnormal corneal responses?
V - Trigeminal
VII - facial
What cranial nerves cause abnormal spontaneous eye movements?
III - oculomotor
IV - Troclear
VI - abducens
What cranial nerves cause abnormal Oculocephalic responses (Doll’s eye)?
III - oculomotor
IV - Troclear
VI - abducens
VIII - vestibulocochlear
What cranial nerves cause abnormal Oculovestibular responses?
III - oculomotor
IV - Troclear
VI - abducens
VIII - vestibulocochlear
What cranial nerves cause abnormal respiratory pattern?
Medullary centre
How do you assess motor function?
Motor response
Muscle tone
tendon reflexes
teachers
What can cause a coma without focal signs?
Anoxic/ ischaemic conditions Metabolic disturbances Intoxications Systemic infections Hyperthermia/ Hypothermia Epilepsy
How do you investigate a patient in a coma?
toxicology screen including alcohol level measure blood sugar and electrolytes access hepatic and renal function acid-base assessment and blood gases measure blood pressure consider carbon monoxide poisoning
What are the potential causes for a coma with minimalism with or without focal signs?
subarachnoid haemorrhage
meningitis
encephalitis
What are the causes of coma with focal brain stem or lateralising cerebral signs?
cerebral tumour
cerebral haemorrhage
cerebral infarction
cerebral abscess
What are the most common causes of a coma that lasts more than five hours?
Drug ingestion +/- alcohol
Hypoxia
Cerebrovascular event
Metabolic disorders - diabetes, hepatic/renal failure, sepsis etc
What are the features of ulnar neuropathy?
Site is most often at elbow, sometimes at wrist
Ulnar distribution numbness - dorsal cutaneous branch
Leads to wasting of small muscles
What is myaethenia gravis?
Where body produces antibodies to post synaptic Ach receptor
Results in decreased effectiveness of Ach
Presents with weakness, fatigue but normal sensation
Weakness often generalised - often eyes
Diplopia/pitosis
How do you diagnose myasthenia gravis?
Detect antibodies
Neurophysiology - repetitive stimulation, single fibre EMG
What is EMG?
Looks for action potentials from whole motor units
SF EMG uses filter, sensitivity and timebase to isolate the action potentials from individual muscle fibres within a motor unit
Can be used to find “jitter”
What is jitter?
In NM junction disease where the tight relationship between two points within the same motor unit is lost
Due to slight delay in polarisation or even block
What can be seen in an EEG?
Epileptic activity
States of consciousness - sleep/stages of sleep
Encephalopathy
How does ulnar neuropathy look like in a nerve conduction test?
Slowing across elbow (conduction sloness due to demylination)
Evidence for conduction block at elbow
Small sensory response from ulnar nerve
Or small but not slowed motor response and normal sensory
Due to nerve root damage - C8 radiculopathy
When wouldn’t you perform a CT scan?
Minor head trauma exclusion criteria
Seizure - MRI usually indicated
What are the contraindications for an MRI?
Cardiac pacemakers, implantable defibrillators, cochlear implants
Moveable metalic implants - aneqrysm clips, heart valves, recent intraabdominal clips
Claustrophobia, pregnancy, tattoos
When would you do a PET scan?
Glucose usage
Increased in tumour, inflammation, infection
What are the traumatic causes of intracranial haemorrhage?
Extradural haematoma
Subdural haematoma (acute or chronic)
Traumatic subarachnoid haemorrhage
Intra-parenchymal contusions
What are the non-traumatic causes of intracrnial haemorrhage?
SAH
ICH
Vascular malformations
What are the cuases of SAH?
ANEURYSM (80%) Trauma Non-aneursymal (peri-mesencephalic) Arteriovenous malformations AVMs Vasculitis Carotid/vertebral artery dissection
What are the risk factors of SAH?
Peak age = 55-60yrs Hypertension Smoking Cocaine Higher incidence in Finland and Japan Family history of SAH
What are the associated conditions of SAH?
Polycystic kidney disease
Ehlers-Danlos syndrome (collagen disorder)
Marfan’s syndrome
How do intracranial signs present?
Focal neurological deficits
Seizures
ECG changes
Reduced level of consciousness, coma, death
What are the common complications of SAH?
Vasospasm >arterial Hydrocephalus >Affects 25% patients >May need permanent CSF diversion – VP shunt Seizures >5-10% of SAH patients Electrolyte abnormalities >Hyponatraemia (30-45%)
How do you prevent vasospasm following SAH?
Nimodipine for 1st 3 weeks following SAH as prophylaxis
Keep well hydrated (at least 3 l/day)
What is arterial vasospasm?
Spasm of cerebral arteries– unclear mechanism
>Blood in subarachnoid space is irritant
>Causes release of inflammatory cytokines
>Results in smooth muscle contraction in vessel wall
>Brain supplied by spastic artery starved of oxygen
>If untreated – leads to stroke i.e. permanent deficit/weakness
What are the risk factors of an intracerebral haemorrhage?
Hypertension
Increasing age
Substance abuse
Underlying lesion – tumour or vascular lesion
Where is the most common place for an intracerebral haemorrhage?
Basal ganglia
What are the symptoms of an intracerebral haemorrhage?
Developing neurological deficit – may be more gradual than in embolic stroke
Contralateral weakness of face / arm / leg
Dysphasia (if bleed in dominant hemisphere - left)
Symptoms due to raised ICP (intracranial pressure)
>Headache
>Vomiting
>Deteriorating conscious level
>Death
How do you treat intracerebral haemorrhage?
After diagnosis on CT
Control BP – avoid systolic BP >180mmHg (may cause further haemorrhage)
If survive the acute phase – intensive stroke rehab leads to the best outcomes
Hemiplegia common – basal ganglia bleeds usually involve the internal capsule
What is arteriovenous malformation?
Abnormal connection between arteries and veins – no capillary bed
?congenital origin – but do enlarge with age
High flow, high pressure – veins not designed to cope with this therefore risk of haemorrhage
May be diagnosed incidentally
What are the risks of arteriovenous malformation?
Risk of bleeding 2-4% per year
Intraparenchymal (most common)
Subarachnoid
How do you treat arteriovenous malformation?
Surgical excision - possible if AVM within non-eloquent brain Endovascular treatment - glue Focused radiotherapy (takes 2 yrs to work)
