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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

supraspinous lig
interspinous lig
ligamentum flavum
epidural space


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

aka posterolateral
most common
compresses travering disc


describe a far lateral prolapse

aka extraforaminal
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.
Neurological deficits


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

neural- burning
vascular- cramping


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

mainly >50s
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)
Osteophyte formation


what is the Tx for cervical spondylosis

-decompressive cervical laminectomy
-cervical foraminotomy


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

older patients
imbalance and disturbance of gait/ falls (due to hypertonia and decreased proprioception)
clumsy hands
incontinence (rare)
non dermatomal pain
jumping legs at night due to hyperreflexia

weakness, spasticity
+ve babinski and hoffmans


what imaging for degenerative cervical myelopathy

MRI gold standard
-disc degeneration
-ligament hypertrophy
-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

brown sequard


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

expressive dysphagia
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

occipital lobe


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

the metencephalon


what separates the cerebrum from the cerebellum

tentorium cerebelli


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
-thermal regulation
-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

mamillary nucleus


what deficiency causes wernickes

B1 (thiamine)


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

lewey bodies
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)
personality changes
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

memory deficits
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
visual hallucinations


what symptoms might a lesion in the cerebellum cause

ipsilateral ataxia
dizziness and vertigo
slurred speech
intention tremor


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

older people


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

Stupp protocol:
-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

pilocytic astrocytoma


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

young adults
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

25-45 y/o's
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

endocrine dysfunction


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

NF 2


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

30-50 y/os
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

sterotatic radiosurgery

microsurgical excision


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

internal carotid
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

anterior choroidal
posterior communicating

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

vertebral artery
posterior communicating


what does the vertebral artery arise from

subclavian artery


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
pontine branches
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

occipital cortex
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

dural sinuses
superficial veins -> superior sagittal sinus
deep veins -> straight sinus


what is a common cause of haemorrhage in young adults

arteriovenous malformation


what causes AVM



what are the clinical features of AVMs

usually asymptomatic
can cause:
-(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

catheter angiography
-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

head trauma
berry aneurysm (most common non traumatic cause)


what increases the risk of a SAH

large aneurysm
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
vitreous haemorrhage


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

endovasuclar coiling
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

surgical excision


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

Extensor response
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

uncal herniation


what diseases are associated with aneurysms

fibromusclar disease
ehlers danlos


what increases risk of aneurysm rupture

old age
previous aneursymal SAH
large aneurysms


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
Atrial fibrillation
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
Memory disturbance


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
Glucose: diabetes
ESR: giant cell arteritis or other vasculitis
ECG: atrial fibrillation
Specific investigations:

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
brocas- expressive
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

any of:
-Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
-Bilateral motor and/or sensory deficit
-Cerebellar dysfunction
-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

occipital lobe


where is the primary motor cortex

precentral gyrus


where is the primary somatosensory cortex

postcentral gyrus


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

occipital lobe


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

parasympathetic fibres
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
3- SOF
4- SOF
5: V1- SOF
V2- foramen rotundum
V3- foramen ovale
6- SOF
7- IAM
8- IAM
9- jugular foramen
10-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
-internuclear ophthamoplegia


what Ix for MS

demyelinating plaques on MRI
oligioclonal bands in CSF on LP


what is the treatment for optic neuritis

IV methylprednisolone
then oral prednisolone
(treat MS)


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

non arteritic:
- >50s
- sudden vision loss
- painless
- unilateral
- VA >6/60
- inferior altitudinal visual field defect
- sectoral hyperaemic disc swelling

- younger
- sudden
- painful
- unilateral
- 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

arteritic :
- temporal artery biopsy (sensitivity low due to skip lesions)

non arteritic:
- BP
- blood sugar
- cup exam
- exclude GCA


Tx for AION

arteritic (GCA):
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)
pulsatile tinnitus
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:
-stroke, syringomyelia
- 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)
Slit lamp
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
adies pupil
orthostatic hypertension


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

bitemporal haemianopias
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

Temporal radiations:
Contralateral superior homonymous quadrantanopia “pie in sky”.
Parietal radiations:
Contralateral inferior homonymous quadrantanopia ”pie in floor”.
Main radiations:
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
-dilated pupil
-accommodation abnormality

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
female predominance
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.
Axillary freckling.
Ophthalmic features:
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

total= 150ml
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

5-15 mmHg


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

usually trauma
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

enlarged ventricles


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
impaires upgaze
raised ICP
gait abnormalities


Ix for hydrocepahlus

full obstetric and post natal Hx
head circumference
fullness of ant fontanelle
dilated scalp veins?
ophthalmic evaluation

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)
downbeat nystagmus
central cord symptoms (due to syringomyelia) - cape like sensory loss of temp and pain, progressive spastic paralysis starting with upper extremities
ataxic gait


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
5. 2+3
6. 2+3+4

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
raised ICP


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.

cluster HA


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?



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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



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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



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A 20-year-old male presented to A&E after being in a car accident. Neurologic evaluation was as follows: he opened his eyes only to the sound of his name, he was able to localize to a painful stimulus but failed to move his arms and legs to command only. When asked where he was his reply was “my house to go"