Flashcards in Neurosurgery Cortex Deck (368):
what is the function of the corticobulbar tracts
contains UMN of the cranial nerves to provide innervation of the face, head and neck
they innervate the cranial motor nuclei bilaterally
(except the hypoglossal nuclei and the lower facial nuclei which are innervates contralaterally only)
explain the differences between a UMN and LMN facial paly
7th CN nucleus in pons
upper half of nucleus= upper half of face and same for lower and lower
upper half of nucleus receive motor input bilaterally, lower half of nucleus recieves only contralateral info
UMN will have paralysis of contralateral lower facial muscles with forehead sparing (as info from other side)= central facial palsy
LMN will have paralysis of the ipsilateral half of the face= bells palsy
what tracts originate from the brainstem and control involuntary movements
what is the role of the vestibulospinal tract, and where does it originate
originates from the vestibular nucleus in the pons
it controls balance and posture by innervating the antigravity muscles (extensor for legs, flexor for arms)
what is the origin and function of the reticulospinal tract
Originates from the reticular formation in the medulla and pons:
The pontine reticulospinal tract facilitate voluntary/reflex responses and increases tone.
The medullary reticulospinal tract inhibits voluntary/reflex responses and decreases tone (think dulling down)
what is the origin and function of the rubrospinal tract
Originates from the red nucleus in the midbrain. It excites flexor muscles and inhibits extensor muscles of the upper body.
what is the origin and function of the tectospinal tract
Originates from the superior colliculus in the midbrain. It co-ordinates movements of head and neck to vision stimuli.
how many vertebrae all together
what does C1 lack
a spinous process or body
what is different about C2
has dens (ondontoid process)
what is different about C3-4
have short and bifid spinous processes
where does the posterior ligament run
within vertebral canal, posterior to the vertebral bodies
what does the ligamentum flavum do
It runs vertically connecting the lamina of adjacent vertebrae. It helps maintain an upright posture and assist straightening the spine after flexion.
where are LP done
what are the layers a needle has to go through in an LP
what is the usual age range for mechanical back pain
when is mechanical back pain worse
morning stiffness which resolves with movement
pain is made worse by prolonged sitting or when rising from a seated position
what can happen when facet joints are hypertrophied
patients will get referred pain from the nerve supplying the facet join that mimics sciatica, but doesn't radiate below the knee
describe a paramedian prolapse
compresses travering disc
describe a far lateral prolapse
compress the exiting nerve
what can a central/ medial herniation cause
lumbar stenosis or if large enough CES
what is radiculopathy
dysfunction of a nerve root causing dermatomal sensory deficit with weakness of the muscle groups supplied by the nerve
what is sciatic pain like
Shooting pain radiating from the buttocks down to the posterior knee/leg. The pain can be exaggerated by coughing or sneezing.
what does a straight leg raise test positive mean
with the patient lying down on their back, lift the patient's leg while the knee is straight. If the angle to which the leg can be raised before eliciting the patient's sciatic pain is <45° then the test is said to be positive.
what are the clinical features of an L5/S1 prolapse disc involing S1 root
Pain along the posterior thigh with radiation to the heel.
Weakness of plantar flexion (on occasion).
Sensory loss in the lateral foot.
Reduced or absent ankle jerk.
what are the clinical features of an L4/5 prolapse affecting L5
Pain along the posterior or posterolateral thigh with radiation to the dorsum of the foot and great toe.
Weakness of dorsiflexion of the toe or foot.
Paraesthesia and numbness of the dorsum of the foot and great toe.
Reflex changes unlikely.
what are the clinical features of an L3/4 prolapse affecting L4
Pain in the anterior thigh.
Wasting of the quadriceps muscle.
Weakness of the quadriceps function and dorsiflexion of foot.
Diminished sensation over anterior thigh, knee and medial aspect of lower leg.
Reduced knee jerk.
what are the indications for a discectomy following a prolapse
Failure of conservative treatment (physiotherapy and analgesia) - First line management
Central disc prolapse: Patients with bilateral sciatica or other features indicating a central disc prolapse, such as sphincter disturbance and diminished perineal sensation, should be investigated promptly.
if what reflex is present does it make it unlikely to be CES
Tx for CES
emergency MRI lumbosacral
If it was due to a herniated disc --> discectomy
If it was due to a fracture --> decompression +\- fixation
If it was due to a hematoma --> evacuation
what are the clinical features of spinal stenosis
Unilateral or bilateral hip, buttocks or lower extremity pain or burning sensation precipitated by standing or back extension and relieved by sitting, lumbar flexion or walking uphill (patients can often develop an “anthropoid posture” which is exaggerated flexion of the waist).
Neurogenic intermittent claudication: leg weakness, tingling and numbness which can be accompanied by paresthesia.
insidious progressive disease
what is sclerotomal
muscle group with the same vascular supply (distribution of symptoms in vascular claudication)
what is the difference in pain in neural and vascular claudication
what investigation to diagnose neurogenic claudication
MRI lumbosacral spine
what is the treatment for neurogenic claudication
If symptoms are tolerable and the walking distance is not significantly affected then conservative treatment is offered first (physiotherapy and analgesia). Symptoms usually worsen slowly in a predictable manner and surgery should be offered electively when the patient’s symptoms become intolerable and oral analgesia is no longer sufficient. Lumbar surgical decompression (lumbar laminectomy) is the preferred surgical treatment.
what is cervical spondylosis and how can it present
a degenerative arthritic process involving the cervical spine
either present as degenerative cervical myelopathy (UMN signs) or radiculopathy (LMN signs).
what is seen radiologically in cervical spondylosis
Narrowing of the disc space (the C5/C6 and C6/C7 levels are the most commonly affected)
what is the Tx for cervical spondylosis
-decompressive cervical laminectomy
what causes myeopathy and what is the result
can result from a spinal cord compression which causes UMN signs with symptoms more prominent in the lower limbs
what are the clinical features of degenerative cervical myelopathy
imbalance and disturbance of gait/ falls (due to hypertonia and decreased proprioception)
non dermatomal pain
jumping legs at night due to hyperreflexia
+ve babinski and hoffmans
what imaging for degenerative cervical myelopathy
MRI gold standard
-spinal cord signal chance
Tx for degenerative cervical myelopathy
decompressive spinal surgery (prevent deterioration)
what is anterior cord syndrome
Cord infarction by the area supplied by the anterior spinal artery.
It produces paralysis and loss of pain and temperature below the level of injury with preserved proprioception and vibration sensation.
where does the contralateral loss of pain and temp begin in brown sequard
1 or 2 segments below the lesion
what causes central cord syndrome
Acute extension injury to already stenotic neck or syringomyelia or tumour
what are the symptoms of central cord syndrome
Predominantly bilateral upper limb weakness>lower limb (the fibers supplying the upper limbs in the lateral corticospinal tracts are more medial to the fibers supplying the lower limbs, hence a lesion in the central cord is more likely to damage the upper limb fibers).
“Cape-like” spinothalamic sensory loss (pain and temperature).
Dorsal Columns preserved.
how do you remember what rubrospinal tract does
think of a bro flexing his biceps
-excites flexors, inhibits extensors of the upper limb
explain decorticate vs decerebrate postures
Corticospinal most dominant motor tract, then ruborospinal
When don’t have corticospinal tract innervation, rubro will take over (flexion of upper limbs)= decorticate
When rubro knocked out reticulo happens (extension of upper and lower limbs)= decerebrate
what posture will result from a lesion above the level of the midbrain
decorticate- rubrospinal in tact as red nucleus in midbrain, cortico not working
what posture will result from a lesion below the midbrain
decerebrate = cortico and rubro tracts not working so reticulo (originates in pons/ medulla) takes over
how does the DCML reach the post central gyrus
decussate in medulla to the contralateral medial leminiscus to reach the primary somatosensory area
describe the 3 order neurones in the DCML
1st order neurone travel from site of excitation to dorsal sensory ganglion in spinal cord root. 2nd enters dorsal column and ascend entirety of cord crossing to the other side then thalamus where it synapses. 3rd – thalamus to post central gyrus
A 30 year old man presented with a stab wound in his back. He has right sided weakness starting at T5 and left sided loss of pinprick sensation and temperature starting at T7.
what cord compression syndrome
A 39-year-old woman presented with severe headaches whenever she sneezed. She also had decreased sensation to pinprick over her upper back, shoulders, and upper arms. Her power in her arms was 2/5 but her lower body power was 5/5.
what spinal cord compression syndrome
syringomyelia (type of central cord syndrome)
what is syringomyelia
when a cysts forms on the spinal cord and compresses it
what are the dural venous sinuses
between the two layers of dura mater
what is the outer layer of dura mater adherent to
what is the cerebellum derived from embryologically
what does the middle frontal gyrus in the frontal lobe do
contains the frontal eye fields which control contralateral voluntary eye movements
what does the inferior frontal gyrus in the frontal lobe do
contains bocas speech area (in the dominant hemisphere)
what does damage to brocas area produce
can comprehend words but produce faulty sentences and phonemic errors
what does damage to the inferior parietal lobule cause
nominal aphasia (problems recalling words, names and numbers
what does the superior temporal gyrus contain
the auditory area of the cortex
wernickes speech area (in dominant hemisphere)
what does damage to wernickes area cause
receptive dysphasia - impaired comprehension, produces jargon 'word salad) but speech fluent
where is the visual cortex
where is the insula
lies deep within the lateral sulcus
what is the role of the limbic system
higher emotional functions
contains major component of the memory system
where is the limbic system
medial hemisphere surface, encircles the corpus callosum
important structure include the cingulate gyrus and the hippocampus
what is the cerebellum derived from embryologically
what separates the cerebrum from the cerebellum
what is the vermis
midline structure which connects the two hemispheres of the cerebellum
what are the three components of the cerebellum and their functions
vestibulocerebellum - receives input from the vestibular organs for the maintenance of balance and coordinating vestibule-ocular reflexes
spinocerebellum- maintains muscle tone and participates in posture and gait
cerebrocerebellum- coordination of voluntary motor activity, corrects any error in the movements to ensure they are smoothly executed
what is scanning dysarthia
when a patient speaks slowly with poor articulation of speech - caused by cerebellar dysfunction
what parts of brain are derived from the diencephalon
what does the thalamus do
involved in maintaining consciousness
modulates motor function- has reciprocal connections with the motor cortex, basal ganglia and cerebellum
is a relay station for all all sensory impulses (e.g. lateral geniculate nucleus is a relay between retina and visual cortex)
what can a thalamic infarction cause
hemiparesis, spontaneous pain, hemichorea, severe impairment of consciousness
what does the hypothalamus do
influences autonomics, endocrine and limbic system
-regulates release of hormones from adenohypophysis
-synthesis ADH and oxytocin (projects to the neurohypophysis)
-regulates feeding and starvation
-contains mamillary nucleus which receives information from the hippocampal formation
what nucleus is affected in wernickes encephalopathy
what deficiency causes wernickes
what characterises korsakoffs
anterograde amnesia and confabulation
how do patients with wernickes present
confusion, ataxia and nystagmus
what do subthalamic lesions cause
contralateral hemiballism (chorea)
subthalamus is closely connected to the basal ganglia
what does the basal ganglia contain
caudate nucleus, putamen and globus pallidus
what is the role of the basal ganglia
exert both excitatory and inhibitory effects of the motor cortex
initiate and facilitate movement
control muscle tone
what do lesions in the basal ganglia cause
alteration in muscle activity or tone
what are alpha-synuclein containing inclusions
present in parkinsons
what gene causes huntigtons
CAG trinucleotide repeats - increase from generation to generation (genetic anticipation)
what five different symptoms do tumours of the CNS present with
progressive focal neurological deficits
HA- worse on lying down, associated with N&V due to increase ICP
gradual cognitive slowing and personality changes
endocrine disturbances in pituitary or hypothalamic tumours
what symptoms might a lesion in the frontal lobe cause
contralateral weakness (motor cortex)
urinary incontinence (micturition inhibition centre)
gaze abnormalities (frontal eye fields)
expressive dysphagia/ aphasia (brocas area)
what symptoms might a lesion in the temporal lobe cause
receptive aphasia/ dysphagia (wernickes area)
contralateral supeiror quadrantopia
what symptoms might a lesion in the parietal lobe cause
contralateral weakness and sensory loss (primary somatosensory cortex)
contralateral inferior quadrantopia
if domininant lobe affected: dyscalculia, dysgraphia, finger agnosia, left and right disorientation
if non dominant lobe affected: neglect (deficit in awareness of one side of body), dressing apraxia and constructional apraxia
what symptoms might a lesion in the occipital lobe cause
contralateral homonymous hemianopia
what symptoms might a lesion in the cerebellum cause
dizziness and vertigo
what is the WHO grading for gliomas
I- no morphological features
II- atypia alone
III- atypia and mitosis
IV- atypia and mitosis with vascular proliferation/ necrosis
what is the most common primary brain tumour
high grade gliomas
what are high grade gliomas
either WHO grade II (anaplastic astrocytomas) or grade IV glioblastoma multiforme (GBM)
of these GBM more frequent
who gets glioblastoma multiforme tumours
where do GBM tumours arise
in cerebral hemispheres - most commonly in temporal, parietal and frontal lobes
what imaging for glioblastomas
seen as heterogeneously enhancing SOL, with areas of necrosis, can have a butterfly appearance
what is done if an MRI shows a high grade glioma
biopsy taken for prognosis and MGMT promoter and methylation test (predictive repsonse alkylating agent chemo (temozolamide)
what is the treatment for gliobastomas
-surgery + radiotherapy +/- chemo (e.g. temozolamide)
can improve median survival to 14 months
what are low grade gliomas
slow growing primary brain tumours
grades I (pilocytic astrocytomas) and II (diffuse astrocytoma/ oligodendrogliomas)
who gets low grade gliomas
children and adults
most common in 2nd and 3rd decades
who gets pilocytic astrocytomas (a type of low grade glioma)
children and young adults
what is the prognosis for a pilocytic astrocyoma
high cure rate after maximal resective surgery +/- adjuvant therapy
what is the most common low grade glioma
what is the histology of a pilocytic astrocytoma
bipolar cells with long hair like projections
where do pilocytic astrocytomas occur
cerebellum and midline structures (thalamus, optic chiasm)
what condition are optic pathway gliomas common in
neurofibromatosis type 1
where do you get diffuse astrocytomas
cerebral hemispheres, esp frontal and temporal lobes
who gets a diffuse astrocytoma and how do they present
are slow growing - can progress to higher grades
commonly present with seizures
what is the treatment for diffuse astrocytomas
maximal resective surgery + chemo/ radiotherapy
can double life expectancy to beyond 15 years
which low grade glioma has the best prognosis
where do you get oligodendrogliomas
affect the frontal lobe of the cerebral hemisphere, white matter, cortex
can invade subarachnoid space
who gets oligodendrogliomas and how do they present
seizures and headaches
what are meningiomas
common benign extra-axial
(external to brain parenchyma) intracranial tumours that grow slowly, are well demarcated and do not usually infiltrate the brain
(originate from arachonid cap cells in arachoid membrane)
who gets meningiomas
elderly patients - 6th/7th decade
females slightly more
NF type 2
childhood radiation exposure
how do meningiomas present
usually asymptomatic and are found incidentally on imaging
if symptoms develop, then it will correlate with the site of the brain that is affected. The most common presenting complaint however is headache then symptoms of increased intra-cranial pressure can follow.
A meningioma in the olfactory groove can lead to Foster Kennedy syndrome which is clinically defined as optic atrophy in the ipsilateral eye and papilloedema in the contralateral eye
what is the difference between micro and macroadenomas (pituitary tumours)
macro larger than 10mm in diameter
are the majority of pituitary tumours malignant or benign
benign - arise from cell types in anterior lobe of pituitary gland
how do most pituitary tumours present
what is the treatment for prolactinomas
dopamine agonists- cabergoline
what is a high dose dexmethasone suppression test used to determine
adrenal or pituirary causes of cortisol excess
high dose will suppress pituitary causes only
what are thyroid hormones like in a thyrotropinoma (pituitary tumour)
TSH high, free T3 and free T4 high
what is used to shrink GH secreting pituitary tumours before surgery
pegvisomant and somatostatin analogues- octreotide
when is radiotherapy used for pituitary tumours
when too large to operate/ growing into cavernous sinus
what tests should you do if you suspect a pituitary tumour
early morning cortisol and prolactin
what are acoustic neuromas/ vestibular schwannomas
benign tumours derived from schwann cells
arise in cerebellopontine angle and affect the vestibular portion of cranial nerve 8
what should you suspect with bilateral accoustic neuromas in the young
what is the pathology of vestibular schwannomas
Verocay bodies can be seen, which are palisading nuclei against a fibrillary background
what is the presentation of an acoustic neuroma
unilateral SNHL, tinnitus and vertigo
if big can have headache
facial pain/ numbness- if CN V involved
what is the management for vestibular schwannomas
serial observation- hearing aid, MRI, neuro exams
what are haemangioblastoma
benign, cystic, highly vascular tumours
develop in posterior fossa
what is the presentation of a haemangioblastoma
cerebral dysfunction (occur in post fossa)
symptoms of raised ICP
associated with von hipple-landau syndrome - multiple haemangiomas which may be symptomatic (retinal angiomas, renal cell carcinoma and phaeochrmomcytoma)
what should GH levels be after oral glucose (100g)
less than 1mg/ml
what definitive test for acromegaly
what does the anterior intracranial circulation arise from
the internal carotids
what does the posterior intracranial circulation arise from
paired vertebral arteries- join to form basilar
what makes up the anterior circulation of the brain
anterior communcicating artery
where does the internal carotid arise from
common carotids at carotid bifurcation (C4)
what is the path of the internal carotid
enters the base of the skull through the carotid canal
transverses the foramen lacerum (does not pass through it)
what are the branches of the internal carotid
terminates into bifurcation into MCA and ACA
what is the path of the ACA
arches over corpus callosum in the longitudinal fissure
what does the ACA supply
medial part of left and right cerebral hemispheres, back to the parietal lobes
most of corpus callosum
anterior limb of internal capsule
part of caudate nucleus
is the MCA or ACA bigger
what is the path of the MCA
extends from the internal carotid to the sylvian fissure
exits fissure onto lateral surface of hemisphere
what does the MCA supply
majority of the lateral hemisphere, basal ganglia and internal capsule
what does the posterior circulation of the brain consist of
what does the vertebral artery arise from
what is the path of the vertebral artery
extends through the transverse foramen of the cervical vertebrae (C6 to C2)
join to form basilar
what is the main branch of the vertebral arteries
posterior inferior cerebellar arteries
what do the posterior inferior cerebellar arteries supply
posteroinferior cerebellar hemispheres
what is the path of the basilar artery
vertebral arteries combine at the base of the pons
courses superiorly towards the midbrain
terminates at interpeduncular cistern - goes into two posterior arteries
what are the branches of the basilar artery
anterior inferior cerebellar artery
superior cerebellar artery
what does the anterior inferior cerebellar artery supply
the anterolateral part of the cerebellum
also gives off the labyrinthine artery which supplies the inner ear
what does the superior cerebellar artery supply
superior aspect of the cerebellum
what is the path f the posterior cerebellar artery
goes backwards towards the occipital lobe
what does the posterior cerebral artery supply
gives of branches to supply the thalamus
what does the posterior communicating artery branch from
the internal carotid
what are the two components of the brains venous system
cerebral veins (superficial and deep)
dural venous sinuses
why do the dural venous sinuses have arachnoid granulations
to allow CSF to be reabsorbed from subarachnoid space into venous system
what is the path of the superior sagittal sinus
(dural sinuses within two layers of dura mater) runs from the anterior aspect of the falx cerebri
terminates at the confluence of sinuses (is joined by straight sinus)
from here blood drains into left and right venous sinuses and then into internal jugular vein
where do cerebral veins drain to
superficial veins -> superior sagittal sinus
deep veins -> straight sinus
what is a common cause of haemorrhage in young adults
what causes AVM
what are the clinical features of AVMs
-(most common) haemorrhage (most commonly intracerebral, but can be intraventricular or subarachnoid aswell)
-2nd= seizures can be generalised or complex partial
-progressive neurological deficit (e.g. slowly progressive hemiparesis (due to local ischaemia- steal phenomenon)
-headaches - unilateral and throbbing/ more generalised
what Ix for AVMs
-shows feeding arteries supplying the nidus and veins draining it
CTA can be used in emergencies
what is seen on Ix of AVMs
tangle of vessels
large feeding artery
large draining veins
what is the management of AVMs
-open craniotomy and excision
if risks of surgery high and AVM small/ deep then stereotactic radiosurgery (takes 1-3 years to work)
if AVM in deep tissue/ eloquent area and inaccessible to surgery then endovascular coiling
observation if very large AVM/ in eloquent areas of the brain
what is the most common cause of sub arachnoid haemorrhage
berry aneurysm (most common non traumatic cause)
what increases the risk of a SAH
location- higher in posterior circulation
FHx of PKD
co-morbidity- smoking, connective tissue disease
what are the clinical features of SAH
sudden onset thunderclap headache - can last hours- days
neck stiffness and photophobia- meningeal irritation
N&V- raised ICP/ meningeal irritation
a third nerve palsy can occur due to posterior communicating artery aneurysm
confusion, seizures, LOC
what runs in the subarachnoid space
CSF and vessels
where do subarachonoid haemorrhages happen
between arachonoid and pia
is an SAH arterial or venous
what investigations for SAH- what is seen
(if CT normal for example if it was delayed after SAH a LP should be done)
CT angiogram gives you a definitive diagnosis, shows location and route for endovascular coiling
CT- hyperdense signal in subarachnoid space
LP- xanthochromia (yellow discolouration of CSF)
what is the management for SAH
craniotomy and microsurgical clipping of aneurysm can be considered if large MCA aneurysm rupturs/ associated clots
what are the common complications of SAH
vasospasm- prolonged arterial contraction, leading to delayed ischaemic neurologicla deficit, 3-14 days post haemorrhage. treated with nimodipine)
re-bleed- 2 weeks post, more common in elderly/ HPTX, managed with surgical clipping/ coiling
what is cavernous malformation
benign vascular lesion in the sinusoidal spaces
are lined by endothelium, separated by elastin
look in a mulberry
no intervening brain parenchyma
are low flow lesions (unlike AVM)
hard to visualise on angiography
can be familial (usually multiple) or sporadic
what are the clinical features of cavernous malformation
progressive neurological deficit
haemorrhage (can be recurrent and cause neuro symptoms. seizures)
what Ix for caverous malformations
CT- good for acute haemorrhage
MRI T2- gold standard (focal popcorn lesion, surrounded by ring of hypo-intensity = hemosiderin deposition)
angiography- not helpful but can rule others out
what management for a cavernous malformation
where is a subdural haemorrhage
between the dura and arachnoid
is a chronic subdural haemorrhage arterial or venous
venous (cerebral bridging veins)
what is the presentation of a chronic subdural haemorrhage
older patients, recurrent low impact trauma
progressive headache and confusion
what is seen on CT in chronic subdural haemorrhage
hypodense crescent shaped appearance (blood is old)
where is an extradural haemorrhage
between skull and dura
what vessels usually causes an extradural haemorrhage
aterial- middle meningeal artery (under pterion)
what is the presentation of an extradural haemorrhage
young patients head trauma
lucid intervals followed by unconsciouness
what is seen on CT in a extradural haemorrhage
hyperdense biconvex lens appearance
what can a subdural hematoma not cross
falx or tentorium
what are the possible symptoms of cerebral hernitation
Cushing’s triad: hypertension, bradycardia and irregular breathing (damage to the medulla from herniation)
Unreactive pupil (uncal herniation) (oculomotor nerve runs close to the uncus- get palsy)
A patient presents unconscious with unilateral pupil mydriasis that does not constrict to light following a car accident. On CT, an intracranial hemorrhage with cerebral herniation. What is the most likely type of herniation
what diseases are associated with aneurysms
what increases risk of aneurysm rupture
previous aneursymal SAH
what is the most common type of cerebral aneurysm causing a SAH
berry aneurysm (aka saccular)
what are fusiform and mycotic aneurysms
fusiform- occur in intracranial (esp basilar and ICA), due to atheromatous degeneration, associated with hypertension
mycotic due to septic emboli
what nerves can an unruptured posterior communication artery aneurysm compress
oculomotor nerve- 3rd nerve palsy (ptsosis, extraocular palsy)
what nerves can an unruptured anterior communication artery aneurysm compress
if large compresses optic chiasm
what symptom can an unruptured basilar artery aneurysm cause
3rd nerve palsy
what is the treatment of aneurysms
if symptomatic can do endovascular coiling/ neurosurgical craniotomy + clipping of the aneurysm
where can a TIA happen
in brain, spinal cord and retina
what are the risk factors for a TIA
Prior TIA or stroke
History of ischaemic heart disease
what are the clinical features of a TIA
Cortical symptoms: facial or limb weakness, sensory disturbance, ...
Speech abnormalities: dysphasia or dysarthria
Visual disturbance: visual field defects or amarousis fugax
Cranial nerve involvement
what score can be used to identify whether patients with a TIA are at low or high risk of developing subsequent cerebrovascular injuries
Scores of 0-3 points to a low risk subsequent stroke and scores >4 are higher risk subsequent strokes.
includes age, BP. clinical features (any other symptoms= 0, speech= 1, limb weakness= 3)
Patients with a score >4 should be referred to a stroke specialist within 24 hours. Patients with a lower risk should be assessed and treated within 7 days of symptoms onset.
what Ix for TIAs
FBC: to identify any blood disorders
Renal function: chronic renal failure
ESR: giant cell arteritis or other vasculitis
ECG: atrial fibrillation
MRI: to look for ischaemic brain damage
Carotid doppler: if carotid stenosis is suspected
what scan to identify a haemorrhagic stroke
what happens biologically when blood supply to brain is cut off
glucose and oxygen transport to neurones decreases. Glutamate and proteolytic enzymes release causes the formation of cerebral oedema and inflammation which would lead to worsening ischaemia to adjacent neurones and widening of the circle of cell death
what is a penumbra
area of non-functioning yet reversible damage to tissue that if left untreated would lead to an irreversible change to the cells.
what are the types of dyspahgia
wernickes - receptive
conductive- damage to the arcuate fasciculus that connects Broca to Wernicke
what are the common visual symptoms of a stroke
contralateral homonymous hemianopia
visual inattention- failure to detect visual stimulus in one half of the visual field when both are testes together, can detect when half tested on their own
decribe the innervation to facial muscles
facial nerve nuclei receive bilateral cortical innervation to upper part of face, contralateral innervation to lower face
what are lacunar infarcts
pure motor or sensory stroke/ an ataxic hemiparesis
what does a total anterior circulation infarct have
1. higher cerebral dysfunction (e.g. dysphagia)
2. homonymous visual defect
3. ipsilateral motor and/ or sensory deficit of at least two areas out of face, arm and leg
what does a partial anterior circulation infarct have
two of TACI features:
1. higher cerebral dysfunction (e.g. dysphagia)
2. homonymous visual defect
3. ipsilateral motor and/ or sensory deficit of at least two areas out of face, arm and leg
what does a posterior circumlocution infarct have
-Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
-Bilateral motor and/or sensory deficit
-Isolated homonymous visual field defect
Tx for ischaemic stroke presenting within 4.5 hrs
intravenous thrombolysis (alteplase). Stroke affecting the carotid territory should be evaluated for carotid endarterectomy.
Some patients with an MCA infarct + cerebral oedema can be considered to be treated with a hemicraniectomy within 48 hours.
Aspirin 300 mg daily should be commenced within hours of ischaemic stroke and continued for two weeks then patients should be transferred to clopidegrol for life (patients who are not suitable for clopidegrol can be put on low dose aspirin (75 mg)+dipyridamole). In Atrial Fibrillation patients, warfarin can be re-introduced after 2 weeks following a major stroke.
what lobes might be affected in an anterior circulation stroke
frontal, parietal and temporal
what is the role of the brain stem
swallowing, breathing, heartbeat, consciouness
what is a role of the parietal lobe
comprehension of language
where is the primary auditory cortex
superior temporal gyrus
where is brocas area
inferior frontal gyrus
where is wernickes area
superior temporal gyrus/ temporo-parietal area
where in brain does thermoregulation
where is the primary visual cortex
where is the primary motor cortex
where is the primary somatosensory cortex
where is the oculumotor nucleus
A 40 year old right-handed accountant presents with difficulty in writing and that he ”wasn’t as good with numbers as before”. On examination, he had a left-right disorientation. Imaging and biopsy confirmed the presence of a meningioma.
where is the lesion
left parietal lobe- gestern syndrome (dominant parietal lobe lesion)
what is a common presentation in cavernous malformations
new onset seizure
what part of brain does the optic nerve transmit to
what branches of optic nerve decussate at chiasm
what comes after the optic chiasm
the optic tracts
what connects the optic tracts to the chiasm
lateral geniculate nucleus
what does the optic tract convey
info from contralateral nasal and ipsilateral temporal retina
left tract will be right side of vision
where do fibres that serve the afferent limb of the pupillomotor reflex exit the optic pathway
leave optic tracts to terminate in the pretectal nuclei in midbrain
then projects to edinger westphal nuclei
what do the optic radiations do
connect the lateral geniculate nuclei to the visual cortex in the occipital lobe
where do the different parts of the optic radiations end up
Superior optic radiations pass through the parietal lobe and end superiorly to the calcarine sulcus
inferior optic radiations (Meyer’s loop) pass through the temporal lobe and end inferiorly to the calcarine sulcus
where is the macula represented in the brain
lateral to the tip of the calcarine sulcus
where is the oculomotor nucleus
located in the dorsal midbrain at the level of the superior colliuculus
what supplies the levator muscle of the eyelid
what is the path of the oculomotor nerve
through the interpeduncular fossa
passes between the posterior cerebral artery and superior cerebellar artery
travels through lateral wall of cavernous sinus
enters orbit through superior orbital fissure
what fibres from the EW nucleus accompany the oculomotor nerve- what do they do
innervate the sphincter papillae and ciliary muscles
where is the troclear nuclei
in midbrain at the level of the inferior colliculus
how does the trochlear nerve enter to orbit
passes through lateral wall of the cavernous sinus inferior to the oculomotor nerve and enters the orbit through the superior orbital fissure
what is unique about the trochlear nerve
It is the only cranial nerve that exits dorsally from the brainstem.
It is the smallest cranial nerve.
Has the longest intracranial course.
what is the course of the abducens nerve
travels through the cavernous sinus lateral to the internal carotid. It then enters the orbit via the superior orbital fissure to innervate the lateral rectus (abduction).
what cranial nerve originates from the telenecephalon
what cranial nerve originates from the diencephalon
what cranial nerves originate from the midbrain
oculomotor and trochlear
what cranial nerves originate from the pons
what cranial nerves originate from the pons at the cerebellopontine angle
what cranial nerves originate from the medulla
what are the cranial origins for each cranial nerve
1- cribiform plate
2- optic canal
5: V1- SOF
V2- foramen rotundum
V3- foramen ovale
9- jugular foramen
11- jugular foramen
12- hypoglassal canal
what is the motor supply of CNV3
muscles of mastication, tensor tympani and tensor veli palatini
what is the motor supply of CN 7
muscles of facial expression (including orbicularis oculi for eye closure) and stapedius muscle.
what is the sensory function of the facial nerve
part of the auricle
what is the special sensory function of the facial nerve
taste to the anterior two-thirds of the tongue (chorda tympani).
what is the parasymp function of the facial nerve
lacrimal gland (greater petrosal nerve) and submandibular/sublingual glands (chorda tympani).
what are the functions of CN 9
Motor supply to stylopharyngeus
Parasympathetic supply to the parotid gland.
Sensory supply to the middle ear and the posterior third of the tongue.
Taste in the posterior third of the tongue
what are the functions of the vagus nerve
Sensory supply to the external ear
Taste over epiglottis
Motor supply to the soft palate, larynx and pharynx.
Parasympathetic supply: bradycardia, peristalsis and vomiting.
what muscles does the accessory nerve supply
SCM and trapezius
what is the path of the pupillary light reflex
Light enters the eye causing signals to be sent along optic nerve. The signals exits the optic tract to the ipsilateral pretectal nucleus in the midbrain. The pretectal nuclei projects bilateral signals to both Edinger-Westphal nuclei.
Pre-ganglionic parasympathetic fibres, from Edinger-Westphal, travels along with the oculomotor nerve then exits to synapse with the post-ganglionic neurons in the ciliary ganglion. From the ciliary ganglion, the parasympathetic fibres are carried via the short ciliary nerves to innervate the ciliary muscle and sphincter pupillae (constrictor).
what is accomodation
focusing on close objects
what are the components of the accommodation reflex
Increase lens curvature: the ciliary muscle contracts (via parasympathetics form Edinger-Westphal) leading to relaxation of the suspensory ligaments of the lens.
Constriction of the pupils: activation of the sphincter pupillae (via parasympathetics form Edinger-Westphal).
Eye convergence: contraction of medial recti via cranial nerve III.
what NT is released in both symp and parasymp ganglions to constrict or dilate the pupil
what is the pathway for pupil constriction
First order neurons: Start at the posterolateral hypothalamus and synapse at the intermediolateral cell column between C8 to T2.
Second order preganglionic neurons: leaves intermediolateral cell column, travels over lung apex and synapse at the superior cervical ganglion at the carotid bifurcation (where sudomotor fibres exits to course with the external carotid and supply the sweat glands of the face).
Third order postganglionic neurons: travels around the internal carotid artery to join the ophthalmic part of the trigeminal nerve. Then enters the ciliary ganglion (does not synapse) to supply the dilator pupillae via long ciliary nerves.
what are the common signs of optic nerve dysfunction
Decrease in visual acuity (VA).
Dyschromatopsia: visual colour impairment (loose red first)
Visual field defects.
Diminished contrast sensitivity.
Relative afferent pupillary defect (RAPD).
what can cause optic neuritis
demyelinating- MS (female predominance, 3rd/4th decade, more common further from equator), neuromyelitis optica (devic disease, bilateral ON, muscle weakness, increased tone and spasm)
what are the clinical features of MS
sensory loss- numbness/ pins and needles
spinal cord symptoms (motor)- muscle cramping and weakness
autonomic features: bladder, bowel, sexual dysfunction
cerebellar: tremor, dysarthria, ataxia (charcots triad)
L'hermitte sign: electric shock on neck flexion
uhthoff phenomenon: worse symptoms due to increase in temperature
-ON: commonly presenting complaint, unilateral pain exacerbated by eye movements, decreased VA, central scotoma, dyschromatopsia, RAPD
what Ix for MS
demyelinating plaques on MRI
oligioclonal bands in CSF on LP
what is the treatment for optic neuritis
then oral prednisolone
what is anterior ischaemic optic neuropathy (AION)
damage to the optic nerve due to ischaemia
can be non arteritic (caused by occulusion of short posterior ciliary artery- idiopathic, HTPx, diabetes, sleep apnoea) or arteritic (GCA causing occlusion of short posterior ciliary artery)
what is the difference in presentations between arteritic and non arteritic AION
- sudden vision loss
- VA >6/60
- inferior altitudinal visual field defect
- sectoral hyperaemic disc swelling
- severe visual loss
- VA <6/60
- scalp tenderness, headache, jaw claudication
-chalk white diffue swollen disc
- optic atrophy (pale disc)
what type of AION causes more risk to the other eye
arteritic (90% is not treated) (GCA)
what investigations for AION
- temporal artery biopsy (sensitivity low due to skip lesions)
- blood sugar
- cup exam
- exclude GCA
Tx for AION
high dose IV methylprednisolone, then oral prednisolone + aspirin (if no CI)
non arteritic: treat cause
what are the symptoms and signs of raised ICP
headache (worse in morning)
deterioration of consciouness
what are the signs and symptoms of papilloedema
symptoms of raised ICP
transient visual loss (lasts seconds)
enlarged blind spot
optic disc signs- hyperaemia, blurred margins of disc (early,
swelling and elevation of the whole optic disc, peripapillary splinter haemorrhages
what is horners syndrome characterised by
ptosis (muller muscle (superior tarsal muscle) dysfunction
ipsilateral anhydrosis (if lesion below superior cervical ganglion)
what causes horners syndrome
lesion in the sympathetic pathway:
- pancoast tumour, carotid aneurysm/ dissection
- ICA dissection, cluster HA, cavernous sinus lesion
- trauma (most common in children)
what does a painful horners syndrome make you think
carotid/ internal carotid artery dissection
what Ix for horners
Apraclonidine can be used to confirm a Horner’s pupil: topical apraclonidine is an alpha-1 receptor agonist which causes pupillary dilation in the Horner's pupil due to denervation hypersensitivity, however, normal pupil remain unaffected.
CT or MRI are used to identify tumours or artery dissection/aneurysm
what is laternal medullary syndrome (wallenbergs syndrome)
occurs due to ischaemia to the lateral part of the medulla oblongata due to blockage of the posterior inferior cerebellar artery or vertebral artery:
-Damage to the vestibular nucleus causing vertigo,vomiting and nystagmus.
-Damage to the descending sympathetic system causing ipsilateral Horner's syndrome.
-Damage to the spinal trigeminal tract causing ipsilateral loss of pain/temperature and loss of corneal reflex.
-Damage to the spinothlalamic tract causing contralateral loss of pain/temperature in the trunk and limbs.
-Other symptoms include dysphagia and horseness.
what is adies pupil
caused by loss of postganglionic parasympathetic innervation to the iris sphincter and ciliary muscle
-more common in females
- usually unilateral
- affected pupil is large
- blurring on near vision (slow constriction on accommodation)
0.125% (low dose) of topical pilocarpine into both eyes. Adie’s pupil constricts (due to denervation hypersensitivity) while normal pupil doesn’t
what is holmes adie syndrome
diminished/ absent deep tendon reflex of lower limbs
what is argyll robertson pupil
caused by diabetes (used to be neurosyphilis)
- characterised by bilateral irregular small pupils
- both pupils accommodate but do not react ;)
-0.1% pilocarpine does not cause constriction (opposite of adies)
what do craniopharyngiomas cause
can cause growth failure, delayed puberty, headaches, diabetes insipidus, obesity and hypothyroidism in children
what visual defect do lesions in the optic tract cause
contralateral homonymous hemianopia
what visual defect do lesions in the optic radiations cause
Contralateral superior homonymous quadrantanopia “pie in sky”.
Contralateral inferior homonymous quadrantanopia ”pie in floor”.
Contralateral homonymous hemianopia.
what visual defect do lesions in the occipital cortex cause
Occlusion of the calcarine artery of the posterior cerebral artery= Contralateral homonymous hemianopia with macular-sparing.
Damage to the tip of the occipital cortex in a posterior head injury= Congruous homonymous macular defects
what are the signs and causes of a 3rd nerve palsy
-abduction and depression in primary position (down and out) with ophthalmoplegia
-only abduction of eye is normal
causes: diabetes, HPTx (both microvascular) - are pupil sparing as blood supply to pupil no affected
posterior communicating artery aneurysm (acute painful), trauma, uncal herniation
what syndrome present with 3rd nerve palsy
webers- stroke affevting ventral midrain: ipsilateral 3rd NP, contralateral hemiparesis (cerebral peduncle)
benedikts- stroke affecting dorsal midbrain, ipsilateral 3rd nerve palsy, contralateral tremor, ataxia, choea (red nucleus)
what are the features and causes of a fourth nerve palsy
Vertical diplopia: worse on walking downstairs or looking down.
Hypertropia: the affected eye is higher than the contralateral eye. It is made worse on tilting the head to the ipsilateral shoulder.
Depression of the eye is limited: most noted on adduction. (SO innervated by CN4- cant look down and out)
Compensatory head tilt: to avoid diplopia, the patients tend to develop a contralateral head tilt.
most common causes: trauma, congenital (can get idiopathic or microvascular)- longst course through skull
what are the features and causes of a 6th nerve palsy
Horizontal double vision: worse on looking at distant targets.
Esotropia in primary position.
Abduction is limited.
causes: microvascular: diabetes, HPTx
raised ICP (herniation of brain stem can stretch CN 6)
what is myasthenia gravis
autoimmune disease of acetylecholine receptors at post synaptic NMJ
presents in 3rd decade of life
affects voluntary muscles and smaller muscles first
occular involvement v high- presenting features
what are the clinical features of MG
Ptosis: typically bilateral (can be unilateral initially) and worse at end of the day/prolonged upgaze.
Cogan lid twitch: brief upshoot of the lid elicited by making patient look downwards then upwards.
Fragility and weakness of muscles of facial expression and proximal limb muscles.
what Ix for MG
Ice test: ptosis improve after applying ice for 2 mins.
Antibodies: anti-ACh Receptor Antibody and anti-Muscle-Specific Kinase (MUSK) Antibody (can be positive in those with –ve anti-AChR).
Electromyograhy and muscle biopsy.
Imaging of thorax: can reveal thymoma as it can be associated with myasthenia.
what treatment for MG
Pyridostigmine (anticholinesterase), steroids and immunomodulators.
Surgery if thymoma is present (thymectomy).
what are the features of myotonic dystrophy
delayed muscular contraction and muscle wasting
Early onset cataract: iridescent dust like opacities on the lens resembling Christmas tree catarct.
what causes myotonic dystrophy
autosomal dominant condition due to tri-nucleotide repeat on chromosome 19
what causes NF 1 and NF2
mutation in the NF1 gene (chromosome 17)- autosomal dominant
NF2 gene (chromosome 22)
what are the clinical features of NF1
Café-au-lait spots: brownish spots most commonly in the trunk.
Optic nerve glioma
Bilateral Lisch nodules: hamartomas pigmented lesions protruding above the iris.
Plexiform neurofibromas of the eyelid: “bag of worm” sensation.
what are the clinical features of NF2
Bilateral/unilateral acoustic neuromas: decreased hearing or tinnitus
what is benign essential blepharospasm
A bilateral idiopathic condition characterized by involuntary contraction of the orbicularis oculi muscle. Typically presents in the sixth decade of life with a female predominance
treated with botox and artificial tears
what does the cavernous sinus contain
within lateral wall- CN 3,4,5 (V1 and 2)
going through sinus= ICA (with sympathetic system) and CN 6
where is the cavernous sinus
lateral to sella turcica
posterior to superior orbital fissure
what can cause cavernous sinus syndrome
infections, tumours, cavernous sinus thrombosis, internal carotid aneurysm and carotid-cavernous fistula
what are the features of cavernous sinus syndrome
Ptosis and ophthalmoplegia: due to compression of cranial nerves 3,4 and 6
Loss of corneal reflex: due to cranial nerve 5 (V1) involvement
Maxillary sensory loss: due to cranial nerve 5 (V2) involvement
Horner's syndrome: due to involvement of internal carotid ocular sympathetics
Proptosis and periorbital swelling: due to increased venous pressure in the veins draining the orbit
explain decoritate posturing and what it means
indicates severe brain damage to areas including the cerebrum, internal capsule and thalamus. The midbrain is generally spared. The patient presents with abnormal flexion of his arms, the hands are clenched into fists, and the legs extended and feet turned inward. This is because the lateral corticospinal tracts are disrupted so the rubrospinal tracts takes over causing the abnormal flexion to the upper extremities and the reticulospinal tracts takes over causing the extension of the legs.
explain decerebrate posturing and what it means
indicates an even more severe brain damage and brainstem damage, specifically at a level below the red nucleus in the midbrain. The patient presents with his head arched back and both arms and legs extended. In this case, both the lateral cortical spinal tract and rubrospinal tract are damage so the reticulospinal tract takes over and causes extension of the whole body.
what is the most significant section of the GCS
motor- drops only when there is a significant neurological issue
what is the total volume of csf and how much is produced daily
produced/ day = 450 ml
what is the path of CSF
flows from the lateral ventricles to the third ventricle via the foramen of Munro (intraventricular foramen). From the third ventricle, the CSF flows through the (cerebral) aqueduct of sylvius to reach the fourth ventricle. The CSF then circulates back to the subarachnoid space through foramina of Magendie and Luschka and is absorbed by the arachnoid granulations back to venous blood
what is the normal ICP range when supine
what happens to cerebral blood flow and prefusion pressure when ICP rises
both drop - can develop to ischaemia, brain swelling and herniation
what is cushings triad of raised ICP
irregular, decreased respiration
what is an uncal herniation
medial temporal lobe herniating through tentorium
what are the symptoms of an uncal herniation
The first symptom is pupillary dilatation due to involvement of the ipsilateral oculomotor nerve.
The herniated uncus further compresses the pyramidal tracts at the crus cerebri, causing contralateral hemiparesis.
what is a subfalcine herniation
herniation of the cingulate gyrus below the falx cerebri
what can a subfalcaine herniation cause
compression of the ipsilateral anterior cerebral artery, causing weakness in lower extremities
what is a tonsilar herniation
displacement of the cerebellar tonsils into the foramen magnum
what can cause a tonsilar herniation
a posterior fossa lesion or an Arnold-Chiari malformation
what are the symptoms of a tonsilar hernation
medullary compression and ischaemia characterized by neck stinfness, abnormal neck posture, respiration anomaly (Cheyne-Stokes breathing; periods of tachypnea and tachycardia followed by periods of bradycardia and bradypnea) and coma.
what can central herniation of the brainstem cause
diplopia due to sixth nerve palsy and brainstem dysfunction
which layers of dura mater exist in the spine
only the meningeal (mot the periosteal)
where are extra and epidural haematomas
between dura and skull
what causes an extraudral haematoma
The separation of the dura from a bone following a shearing stress (head trauma) with the disruption of vessels causes the expansion of the haematoma.
The most common source of bleeding is from the disruption of the middle meningeal artery (the anterior branch of the middle meningeal artery is vulnerable to injury as it runs underneath the pterion) most commonly associated with a temporoparietal skull fracture.
The most common location for an EDH is the temporoparietal region but it can occur less commonly in the frontal, occipital or posterior fossa regions.
what are the symptoms of an extradural haematoma
young adult sustaining a closed head trauma. The classic symptoms include a brief loss of consciousness, followed by a period in which the patient regains consciousness and awareness (called a lucid interval), after that the patients further deteriorates, exhibiting symptoms such as: headache, vomiting, contralateral hemiparesis (due to compression of the cerebral peduncle) and ipsilateral pupillary dilatation (the expanding haematoma causes the uncus of the temporal lobe to herniate and compress on the pupillary fibres of the oculomotor nerve).
Unlike subdural haematomas, the rapidity of the decline occurs as the expanding haematoma are from a high pressure arterial source, rather than from the low pressure venous system
what Ix for extradural haematomas
will see lens (lemon) shaped haematoma +/- mass effect/ herniation
why is an extradural haematoma lens/ lemon shaped
as periosteal dura stuck to bone, blood can get over sutures
Tx for extradural haematomas
for expanding extradural hematomas is immediate neurosurgical evacuation of the haematoma if there is significant or ongoing neurological deficit.
Conservative management is sometimes considered in neurologically intact patients with a small extradural haematoma.
what is the presentation of a subdural haematoma
Most SDHs presents unilaterally in adults. However, bilateral SDHs are more common in children owing to the absence of adhesions in the subdural space which develop with ageing.
Acute SDH forms quickly and the patient becomes symptomatic immediately= severely decreased state of consciousness. Some patients can still remain conscious until the haematoma expands more and then deteriorate.
Chronic SDH, on the other hand, takes a longer time course, with a mean of 3-7 weeks before symptoms starts to present= headache and confusion. Other symptoms include: urinary incontinence, weakness, seizures, cognitive dysfunctions and gait abnormalities
what is the pathophysiology of acute SDH
The acceleration/deceleration mechanism the brain is subjected to after a high impact trauma to the head, results in the rupturing of bridging veins (veins that drain the cotex and empty in dural sinuses). Cerebral blood flow can also be reduced and the blood volume in the brain decreases as a result from compression with midline shift and cerebral oedema due to increased Intracranial pressure
what is the pathophysiolgy of a chornic SDH
brain atrophy main driving factor- due to age, chronic alcoholism or dementia (bridging veins are stretched and even minor trauma can cause them to rupture)
The leaky vessels result in the accumulation of blood in the subdural space and an osmotic gradient can form which draws more fluid in that space. The ICP then rises dramatically causing a decreased blood perfusion in the brain thus, the patient becomes symptomatic
Other predisposing factors is the use of anticoagulation, such as aspirin, which causes continued and non-stopped bleeding into the subdural space
or due to inflammationand angiogenesis- Following a traumatic head injury, inflammatory cells are recruited forming new membranes and activate inflammation. Angiogenesis also causes the formation of fragile leaky vessels within the membrane causing more blood and fluid accumulation
what imaging for a SDHaematoma
acute SDH- cresent shaped hypersensity
chronic SDH- hypOdense cresent shape
what is normal pressure hydrocephalus
the buildup of CSF due to impaired resorption at the arachnoid granulations/ overproduction of CSF
mostly idiopathic, can be caused by trauma, meningitis or SAH
increased CSF but CSF pressure within normal range (does fluctauate and have nocturnal peaks)
what does LP show in normal pressure hydrocephalus
normal opening pressure
what are the clinical features of normal pressure hydrocephalus
apraxia of gait (commonly presenting symptom) = shuffling gait
dementia (can be reversible)
urinary incontinence (over activity of detrusor muscle due to reduced/ asbent central inhibition)
what will be seen on imaging in normal pressure hydrocephalus
what is the treatment for normal pressure hydrocephalus
ventriculo-peritoneal shunt (reserved for patients with marked ventriculomegaly with severe symptoms/ marked improvement after removal of CSF)
what is hydrocephalus
excessive accumulation of CSF leading to enlarged ventricles
what are the types of hydrocephalus
communicating or non communicating:
-communicating= no obstruction of flow between ventricles and sub arachnoid space. reduced absorption due to impaired arachnoid granulations
-non communicating= obstruction in ventricular system (can usually tell by seeing if 4th ventricle small or not- if small NC) caused by tumour, colloid cyst (3rd ventricle), stenosis of aqueducts
congenital or acquired:
congenital= aqueductal stenosis (most common), type 2 arnold chiari malformations, spina bifida, dandy walker syndrome
- acquired= tumours, infections, trauma
what are the symptoms of congenital hydrocephalus
failure to thrive
dilated scalp veins
increased head circumference
impaired upgaze due to compression on tectal plate
setting sun sign (downward deviation of the globe on lid retraction)
raised ICP and diplopia (6th nerve palsy)
macewan sign 'cracked pot' sound on head percussion
what are the symptoms of acquired hydrocephalus
HA- worse in mornings
Ix for hydrocepahlus
full obstetric and post natal Hx
fullness of ant fontanelle
dilated scalp veins?
MRI best to find cause and site of obstruction
CT used in acute setting
management for hydrocephalus
venticulomegaly + raised ICP= need CSF diversion asap
- VP shunt (allows CSF to be absorbed outside CNS)
- endoscopic 3rd ventriculostomy (creates direct pathway from 3rd V to basal cisterns + SAS- only works in non communicating as needs working absorption)
what are chiari malformations
congenital/ acquired malformations of the hindbrain - affects cerebellum, medulla and upper cervical spinal cord structural relationships = causes impaired SF circulation through the foramen magnum
what is a chiari I malformation
(most common + least severe)
- caudal displacement of the cerebellar tonsils below FM
-may be associated syringomyelia (expanding cystic cavity or syrinx in spinal cord that damages it)
causes HA (worse when coughing) with suboccipital pain (can be brought on by neck extension)
central cord symptoms (due to syringomyelia) - cape like sensory loss of temp and pain, progressive spastic paralysis starting with upper extremities
what is a chiari II malformation
(less common more severe)
happens more in children
caudal displacement of cerbellum AND medulla below FM with herniation of the 4th ventricle
associated with spina bifida
hydrocephalus and syringomyelia also common
patients present in infancy/ childhood:
-severe brain stem dysfunction in infants- dysphagia, apnoea, stridor, nystagmus
-weakness that may progress to quadriplegia
management of chiari malformations
surgical or conservative
Suboccipital craniectomy and upper cervical laminectomy to decompress the malformation at the foramen magnum are usually required with cord drainage
aims to restore flow of spinal fluid
what is pseudo tumour cerebri/ benign intracranial hypertension
idiopathic intracranial hypertension
(idiopathic disease that occurs when there is raised intracranial pressure with the absence of any space-occupying lesions or hydrocephalus. It occurs at a higher incidence in young females and obese patients)
what are the clinical features of IIH
Headache: throbbing type which is worst first thing in the morning and is relieved on standing.
Moderate or gross bilateral papilloedema.
Nausea and vomiting.
Less commonly, sixth nerve palsy can occur due to increased intracranial pressure.
what Ix for IIH
CT or MRI: shows a normal or reduced size of ventricles (“slit-like” ventricles).
Visual field testing and fundoycopic examination for papilloedema.
Lumbar puncture, if not contra-indicated.
what is the management for IIH
initially medical with weight loss (if obese) and diuretics, such as acetazolamide, to help reduce the intracranial pressure.
Surgical intervention include CSF diversion techniques such as a lumbo-peritoneal shunt.
Which one of the following is NHS standard of care for a symptomatic, easily accessible glioblastoma in a young, fit patient?
1. Biopsy only
2. Radiotherapy only
3. Temozolomide chemotherapy only
4. Maximal surgical debulking surgery only
6- radio, chemo and maximal surgical debulking
A 6-month-old girl presented with a head circumference rising from the 66th to the 99th percentile and failure to thrive. On examination, when the lids are retracted, the eyes look like they are sunsetting, and upward gaze is impaired.
a) Non-communicating hydrocephalus due to arnold-chiari
b) Non-communicating hydrocephalus due to aqueduct stenosis
c) Communicating hydrocephalus due to arachnoid granulation dysfunction
d) Communicating hydrocephalus due to a colloid cyst
Non communicating (Most common cause of this is aqueduct stenosis)
A 75 year old patient presents with a progressive shuffling gait and urinary incontinence. He denies any back pain. His wife is claiming that he has been forgetting his keys and taking his medication. What is the most likely diagnosis?
a) Chronic subdural haematoma
b) Cauda equina syndrome
c) Normal pressure hydrocephalus
d) Ischaemic stroke
normal pressure hydrocephalus
gait disturbance, ataxia, dementia, urinary incontinence presenting acutely in the elderly
A 56-year-old man presents with a headache, severity 8/10 with associated nausea. On examination he has ptosis, and miosis.
internal carotid dissection (causing horners syndrome)
A 56-year-old man presents with a progressive headache, severity 6/10 with associated nausea. On examination he has ptosis, and a right dilated unreactive eye
posterior communicating aneurysm (causing a 3rd nerve palsy)
A 56-year-old man presents with a headache, severity 10/10 with associated vomiting. On examination he has neck stiffness and photophobia
A 40-year-old obese lady on the contraceptive pill develops headaches first thing in the morning which are worse on coughing. She is complaining of double vision. What could be causing her diplopia?
6th nerve palsy- causes: microvascular: diabetes, HPTx
A 55 year old man develops diplopia after a closed head injury accident. He says the diplopia is worse when he is going down the stairs. On examination, you see he has a head tilt to the right.
4th nerve palsy- trauma
A patient develops retro-orbital pain in his right eye described as a boring, worst pain he has ever felt, lasting 20 minutes. Associated tearing of that eye and a stuffy nose. He has 10 episodes of this pain for the past week.
A 30-year-old female presented with double vision and ataxia. Three years earlier she had an episode where she lost vision in her left eye for two weeks. On exam, she was mildly ataxic, with brisk reflexes, and both horizontal and vertical nystagmus. What is the most likely diagnosis?
calculate the GCS score:
A 25-year-old man developed a severe headache and collapsed. Upon calling his name, he does not respond nor opens his eyes. However, when a painful stimulus is applied he internally rotates his shoulders and flexes his forearm and wrists while extending his legs
Calculate the GCS score:
A 70-year-old woman presents with a headache and confusion, 4 weeks after she suffered from a fall. She opens her eyes spontaneously and moves her arms and legs when told to