Neuro Flashcards
action pons vs medulla vs midbrain
pons- feeding and sleep
medulla- cvs and resp
midbrain- reflex eye responses
fasiculus vs funinculus vs tract
fasciculus- subdivision of a tract supplying a distinct region of the body
funiculus- a segment of white matter containing multiple distinct tracts. bidirectional
tract- white matter pathway connnecting two regions of grey matter
gracile vs cuneate fasiculus
gracile- lower
cuneate- upper
3 types of fibres and roles
association- same hemisphere
projection- to spinal cord
commisural- to other hemisphere
pre vs post central gyrus
pre- motor
post- sensory
purple- cingulate gyrus. emotion and memory
red- corpus callosum. fibres connecting two cerebral hemispheres
green- thalamus. sensory relay station projecting to sensory cortex
blue- hypothalamus. homeostasis
yellow- fornix. output pathway from hippocampus
brown- tectum. dorsal part of midbrain involved in involuntary responses to auditory and visual stimuli
cerebellar tonsils- cerebellum that can herniate and compress the medulla
yellow- parahuppocampal gyrus. key cortical region for memory encoding.
red- optic chiasm. where visual fibres cross over
green- uncus. part of temporal lobe that can herniate, compressing the midbrain
blue- medullary pyramids. location of descending motor fibres.
abnormal neural tube deficits
-craniorachischisis- neural tube remains open,brain and spinal cord don’t form. incompatible with life
-anecephaly- cranial neural tube fails to close. failure of brain to form. may live for a little
-myelocoele- spinal cord does not develop, csf filled cyst. have neurological defects and have meningitis often
which word shows neuro type defecit is present
myelo
normal neuro tube defects
-myelomeningocoele- CSF filled cyst containing spinal cord. does not transilluminate. neurological defect
-meningocoele- CFS filled cyst. transilluminates. no neurological defect
-spina bifida occulta- lack of posterior vertebral arch, tuft of hair/naevus over deficit. no neurological problems.
why do neural tube defects predispose to hydrocephalus
- cord is tethered at site of defect
- as spine grows cord cannot move within vertebral canal, causing brainstem to be pulled down through foramen magnum and become occluded
why does the Caudia equine form
⇒ A 3 months, the spinal cord is the same length as the vertebral column
⇒ Thereafter, the vertebral column grows faster
⇒ The spinal roots must elongate in order to exit at their intervertebral foramen
⇒ Cauda equina is formed
primary vesicles and what secondary vesicles they form
Prosencephalon (Embryonic forebrain)
-
telencephalon and diencephalon
- telencephalon forms cerebral hemispheres
- diencephalon forms thalamus
Mesencephalon (Embryonic midbrain)
-
Mesencephalon
- Forms midbrain
Rhombencephalon (Embryonic hindbrain)
-
Metencephalon and myelencephalon
- metencephalon forms pons and cerebellum
- myelencephalon forms medulla oblongata
what vesicles form which ventricles
LV- Telencephalon
3rd- Diencephalon
CA- Mesencephalon
4th- Meten/myelencephalon
where does the MCA supply
Cortical branches emerge from the lateral fissure to supply the lateral
aspect of the cerebral hemisphere (cortex and underlying white matter), including lateral parts of the frontal and parietal lobes as well as the superior temporal lobe
Deep branches (the lenticulostriate arteries) supply deep grey matter
structures including the lentiform nucleus and caudate as well as the internal capsule
where does the ACA supply
Cortical branches supply the medial aspect of the frontal and parietal
lobes (not the occipital lobe)
There are also branches to the corpus callosum itself as the ACA loops over the corpus callosum as it sends branches to the adjacent cortex
where does the PCA supply
o Supplies occipital lobe, inferior temporal lobe and
thalamus (via thalamoperforator and thalamogeniculate branches)
o Also supplies midbrain en passant
branches of the PCA
o Posterior communicating arteries branch from these to
connect with the anterior circulation (internal carotid artery)
• Superior cerebellar artery supplies the superior aspect of the
cerebellum and midbrain en passant
• Pontine arteries supply the pons (including descending
corticospinal fibres)
• Anterior inferior cerebellar artery the supplies the antero-
inferior aspect of the cerebellum and lateral pons en passant
draw circle of willis
compare the regions of the body supplied by MCA/ACA
mca- upper limb
aca- lowe limb
describe blood supply to the spinal cord
anterior 2/3- ASA
posterior 1/3- PSA
describe blood supply to CST, STT and DCML
CST/STT- anterior spinal
DCML- posterior spinal
compare PSA and ASA blockage
PSA
- unilateral as the arteries are paired
- ipsilateral loss of DCML below level
ASA
-midline arteries so effects are bilateral
-loss of STT below level and UMN signs above level due to CST blockage
amacrine
ganglion
horizontal
bipolar
amacrine- inhibitory neurons and project their dendrites to the inner plexiform layer to interact with retinal ganglion cells and/or bipolar cells
ganglion- a type of neuron in the retina which receives visual information from photoreceptors via bipolar cells and amacrine cells
horizontal- laterally interconnecting neurons which help integrate and regulate the input from multiple photoreceptor cells
bipolar- cells which exist between photoreceptors in the retina and act indirectly/directly to transmit signals from the photoreceptors to the ganglion cells
left monocular blindness
left hand side optic nerve lesion
bitemporal hemianopoa
optic chiasm
left hand side homonymous hemianopia
right hand side optic tract
left homonymous inferior quadrantinopia
right superior optic radiation
describe macula sparing
in PCA stroke, the occipital lobe is lost
the MCA supplies the occupital pole and so macula vision is spared
where fo the afferent (CNII) nerve synapse
pre tectal area
3 aspects of accomodation reflex
- Convergence (medial rectus)
- Pupillary Constriction (constrictor pupillae)
- Convexity of the lens to increase refractive power (ciliary muscle)
compare dcml and stt
dcml- lower body medial and upper body lateral
in PSC- lower body medial, upper body lateral
stt- lower body lateral and upper body medial
in PSC- lower body medial, upper body lateral
symptoms brown sequard
sensory
- ipsilateral segmental anaesthesia and dcml loss
- contralateral stt loss
motor
- CST lesion: ipsilateral spastic paralysis (due to loss of moderation by the UMN).
- At the level of the lesion, there will be flaccid paralysis of the muscles supplied by the nerve of that level (since lower motor neurons are affected at the level of the lesion).
receptive field and visual acuity
receptive field- area supplied by a single primary sensory neurone
visual acuity- ability to have two point discirmination
inversely proportionate
where are the cell bodies for primary, secondary and tertiary sensory neurones
primary- dorsal root ganglion
secondary- medulla/dorsal horn
tertiary- thalamus
DCML tract
- first order neurone has cell body in DRG. ascends through gracile (lower) or cuneate (upper) fasiculus
- in medulla synapses with secondary neurone. projected to thalamus
- at thalamus projects to PSC
lower body = medial
upper body = lateral
STT
- first order neurone has cell body in DRG. synapses with second order neurone in dorsal horn, which decussates at ventral white commisure
- second order neurone ascends to thalamus, synapses with third order neurone
- projects to psc
lower body = lateral
upper body = medial
pain modulation
C fibres detect pain, AD fibres are inhibitory interneurones activated my mechano receptors.
Additionally, these encephalinergic interneurones can also be activated by
descending inputs from higher centres such as the periaqueductal grey matter or the nucleus raphe magnus
cell bodies LMN vs UMN
UMN- primary motor cortex
LMN- ventral spinal cord, motor nuclei in brainstem
describe route the UMN takes to LMN
corona radiata
internal capsule
cerebral peduncles (midbrain)
pons
medullary pyramids
decussates
ventral horn
topographical representation in CST compared to motor homunculus
in CST- lower limb lateral, upper limb medial
in motor homunculus- lower limb medial, upper limb lateral
what do the ventral and lateral CST supply
ventral(15%)- proximal
lateral (85%)- distal
what tract do the UMN supplying face go in
corticobulbar
MIDBRAIN
1- CNII and EDW nucleus
- medial lemniscus
- periaquaductal grey matter
- cerebral aquaduct
- superior colliculus
- red nucleus
- substandia nigra
- cerebral peduncles
green- corticospinal tract
pink- thalamic radiations. contaim ascending third order sensory neurones.
blue- corticofugal fibres. from cortex away from brain
yellow- corticobulbar tract
purple- genu
what is the internal capsule
bidirectional white matter pathway containing ascending tertiary sensory fibres and descending UMN motor fibres
action of cerebral peduncles, red nucleus and superior colliculus
cerebral peduncles- connect cerebral hemispheres to midbrain
red nucleus- motor control
superior colliculus- visual reflexes
effects of direct and indirect pathways normally and under influence of dopamine
indirect
- normally inhibitory
- under dopamine at d2, inhibition is inhibited and so it is stimulatory
direct
- normally stimulatory
- under dopamine at d1, excitation is increased.
why is the indirect pathway excitatory under dopamine?
the SNc releases dopamine which inhibits the putamen at D2
this inhibits the normal inhibition of the GPe and so increases GPe activity
this increases the GPe inhibition of STN, and so STN activity decreases.
this decreases STN activation of GPI, and so there is less GPi inhibition of the thalamus.
this increases overall cortical activity
why is the direct pathway excitatory under dopamine
the SNc excites the putamen at D1
this increases inhibition of the GPi
this then reduces GPi inhibiton of the thalamus
this increases cortical activity
what makes up striatum and lentiform nucleus
striatum- caudate nucleus and putamen
lentiform nucleus- putamen and GPi/GPe
where is the lesion parkinsons/huntingtons/hemiballismus
parkinsons- the SNc
hemiballismus-STN
huntingtons- loss of inhibitory projections from striatum to GPe
pathophysiology of parkinsons
loss of dopaminergic neurones in SNc
less activation of direct pathway via D1
less inhibition of indirect pathway via D2
symptoms parkinsons
bradykinesia, rigidity, tremor, hypophonia, micrographia, incontenence, mood changes, dementia
pathophysiology of huntingtons
- loss of inhibiory fibres from striatum to GPe
- Gpe not inhibited and so more inhibition of STN.
this means less activation of GPi and so less inhibition of thalamus from GPi
symptoms huntingtons
chorea, dystonia, loss coordination, cognitive decline
pathophysiology hemiballismus
loss of STN.
less activation of GPi.
less thalamic inhibiton from GPi
more cortical activation
why is unilateral basal ganglia damage contralateral, whereas unilateral cerebellar damage is ipsilateral
basal ganglia- only the CST decussates
cerebellum- the CST and the rubrospial tract deucssate.
inputs and outputs to cortex
inputs- thalamus and cortical areas
outputs-
association fibres eg. arcuate fasiculus
projection fibres eg. UMN
commisural fibres eg. corpus callosum
describe long term potentiaion
- changes in glutamate receptors
- synaptic strengthening
- axonal sprouting
describe strorage of short and long term memories
short- cortical circuits
long term- cerebellum for non declerative
cerebral cortex for declerative
3 outputs from reticular formation
hypothalamus sends histaminergic
thalamus sends glutaminergic
basal forebrain sends cholinergic
EEG trace for different levels of sleep
Awake- beta
Drowsy- alpha
I- theta
II/III- sleep spindles (high frequency outbursts) and K+ complexes (intrinsic rate thalamus)
IV- delta
REM- beta
what does EEG measure
combined activity of neurones. detects neuronal synchrony
3 sleep disorders
narcolepsy, sleep apnoea, insomnia
transtentorial herniation
medial parohippocampal gyrus/uncus herniates through tentorial notch.
causes CNIII lesion and disuption in blood supply from the PCA and the superior cerebellar arteries, also motor signs as cerebral peduncle compressed
tonsillar herniation
the cerebellar tonsils through foramen magnum
subfalcrine herniation
the cingulate gyrus under falx cerebri
- displaces corpus callosum and lateral ventricle
- ACA compressed so ischemia of medial frontal and parietal lobes
what is a water shed area
– areas that lie at most distal portion of artery territory (border MCA and ACA high risk) – wedge shaped necrosis. Seen after hypotensive episode.
cause stroke
Hypertension – 60yrs +, rupture of small intraparenchymal
blood vessels.
Cerebral amyloid angiopathy
Arteriovenous and cavernous malformations
Tumours
effects of hypertension on brain
- Arteriosclerosis (thickened walls) of:
- Deep penetrating arteries and arterioles:
(1) Basal ganglia and thalamus
(2) White matter
(3) Brainstem
what is cerebral amyloid angiopathy, what casues it, effects of it
- Amyloid deposition in the walls of small and medium sized meningeal
and cortical vessels (congo red stain). causes rigid and inflexible and weakens wall, amd risk of haemorrhage. - caused by advancing age, lobar haemorrhages involving the cerebral cortices and tiny
microhaemorrhages.
Arteriovenous malformation
– most common, M>F 10-30 yrs age
- subarachnoid vessels to brain / vessels within the brain.
- wormlike (tangled) vascular channel
Cavernous malformations
– loose vascular channels, distended, thin
walled.
- cerebellum and pons
Capillary telangiectasia
microscopic foci of dilated thin walled
vessels
Venous angioma
dilated venous channels
5 types CNS tumours
- glioma eg. astrocytic
- parenchymal eg. germ cell
- meningeal eg. meningioma
- neuronal eg. ganglion cell
- poorly differentiated eg. medulloblastoma
lymphomas
Diffuse, large B cell lymphomas, associated with pt with
EBV
Germ cell tumours
midline tumours, pineal and suprasellar e.g.
germinoma
• Medulloblastoma
20% Children, cerebellum, radiosensitive.
Meningiomas
benign, derived from arachnoid meningothelial cells,
can cause problems if compress important structure / enlarge.
bacteria causing meningitis
infants- e coli
toddlers- h influenze
young adults- strep pneumoniae
chronic- mycobacterium tuberculosis
bacteria causing cerebral abscess and empyema
abscess- streptococci/staphylococci
empyema- staphylocicci/anerobic gram negative
cause encephalitis
Temporal lobe – HZV
Spinal cord MN – Polio
Brainstem - Rabies
concequences of prion disease
Neuron cell death
Synapse loss
Microvacuolations (spongiform)
Lack of inflammation
cause migraine
trigeminal neuralgia, sensitised to otherwise ignored stimuli. causes vasodilation of cerebral blood vessels
cause and presentation cluster headache
- hypothalamic activation with secondary trigeminal and autonomic involvement
- sharp stabbing unilateral pain around eye. ipsilateral autonomic features
SNOOP
- *S**ystemic
- *N**eurological
- *O**nset is new and above 55
- *O**nset is thunderclap
- *P**apilloedema, postiona, exercise
cause and presenation giant cell arteitis
vasculitis in large and medium sized arteries, usually temporal
sudden onset jaw claudication with headache and visual disturbances. can cause visual loss due to disruption to CNII blood supply
cause and presentation trigeminal neuralgia
compression of CNV by loop of blood vessel
pain in 1+ CNV division, stabbing unilateral facial pain that is triggered by chewing or similar activities or by touching affected areas on the face
reversible causes of dementia
hypothyroidiam, hypercalcaemia, B12 deficiency
changes to brain in dementia
global cortical atrophy, sulcal widening, ventricular dilation
describe beta amyloid plaques
amyloid precursor broken down by beta secretase, forms insoluble plaques
these cause
- amyloid angiopathy that weakens blood vessels
- inflammation causing neuronal death
- reduction in neuronal transmission
patho lewy body dementia
alpha synuclein protein incorrectly broken down and forms lewy body deposits in substantia nigra and cortex.
specific lewy body symptoms
hallucinations, REM sleep disturbance, falls due to parkinsonism
specific symptoms frontotemporal dementia
behaviour disinhibition, innapropriate social behaviour, loss motivation, broca’s aphasia
treatment dementia
acetylcholinesterase inhibitors- donepezil
NMDA antagonists- memantine
cause delerium
B12 deficiency, stroke, infections, withdrawal
ACA
incontenence
CL lower body motor and sensory loss
dysarthia
apraxia
alien hand syndrome
MCA stroke
proximal
- hemiparesis CL
- CL upper body sensory loss
- global aphasia
- CL homonymous hemianopia
Distal
S - CL motor loss and expressive dysphasia
I- Cl sensory loss, Cl HH, and receptive dysphasia
Lacunar
pure sensory/motor or sensorimotor
PCA stroke
Cl sensory loss, HH w macula sparing
brainstem stroke
CL motor and IL cranial nerves
Cerebellar
IL horners and cerbellar signs
CL sensory
basillar
distal- hallucinations, somlomence, CNIII
proximal- locked im
PACS/TACS vs POCS
PACS/TACS
- visulospatial, HH, CL motor/sensory, aphasia
POCS
- cranial nerves, bilateral motor/sensory, conugate eye movemen, cerebeller signs, HH w/ macula sparing
lumbar puncture in subarachnoid haemorrhage
increased opening pressure
xanthochromia
increased protein
high red cell
WCC and glucose normal
ACA vs PCA specific effects on other structures
ACA- optic chiasm, pituitary, frontal
PCA- CNIII palsy
xray raised ICP
midline shift, ventricular effacement, loss grey/white matter differentiation
describe limis to cerebral autoregulation
below 50mmHg cannot vasodilate more, above 150mmHg cannot vasoconstrict more
equation CPP
CPP = MAP- ICP
cushings triad
widened pulse pressure, bradycardia, and irregular respirations
poor prognostic factor
areas involved in limbic system
amygdala, septal area, pre frontal cortex, hipppocampal area, cingulate gyrus
role hippocampus limbic syste
o Receives inputs from many parts of the cortex and processes their emotional content
o projects to the thalamus and also to the hypothalamus (causing autonomic features of emotional responses, since the hypothalamus send projections down through the cord to autonomic preganglionic neurones – the hypothalamospinal tract. This will lead to sympathetic nervous system activation, as well as release of adrenaline from the adrenal medulla – the acute stress response)
o Role in memory – already discussed
role amygdala
o Receives many inputs from the sensory system
o Major outputs to cortex and hypothalamus o Like the hippocampus, involved in behavioural and autonomic emotional responses
role prefrontal cortex
o Modulation of emotional responses (e.g. consciously suppressing features of anxiety)
o ‘Perception’ of emotion
describe HPA axis
hypothalamuc releases CRH
pituitary releases ACTH
adrenal medulla releases noradrenaline, adrenal cortex releases cortisol
treatment PTSD
treatment
Biological
• SSRIs • Maybe short term benzodiazepines
Psychological
• CBT • Eye movement desensitization reprocessing therapy
pathophysiology PTSD
• Evidence of amygdala hyperactivity causing exaggerated
behavioural responses
• However, low levels of cortisol!
patho OCD
- basal ganglia re entry due to direct pathway overactivity
- reduced SSRIs
- autoimmune- PANDAS (post strep)
treatment OCD
Biological
• SSRIs +/- antipsychotics
• Deep brain stimulation?
Psychological
• CBT and variety of other interventions
symptoms anxiety
smptoms – primarily attributable to sympathetic activation
Palpitations
Sweating
Trembling or shaking
Dry mouth
Difficulty breathing
Chest pain or discomfort
Nausea or abdominal distress (e.g. butterflies in stomach)
Feeling dizzy, unsteady, faint or light-headed
patho and treatment anxiety
- low GABA and serotonin
- short term benzodiazapines, SSRIs
actions cortisol
supress immune, allergic and inflammatory responses
increase energy metabolite
general adaptation syndrome
o Stage 1: The alarm reaction
Release of adrenaline and cortisol as well as sympathetic activation (described above)
o Stage 2: Resistance (effect of adrenaline starts to wear off) Chronic stress response, prolonged release of cortisol
o Stage 3: Exhaustion (when you cannot escape an ongoing stressor) Chronic side effects of prolonged cortisol secretion start to occur
mesolimbic pathway
from ventral tegmental area to the limbic structures and nucleus acumbens
mesocortical pathway
ventral tegmental area to frontal cortex and cingulate cortex
brain changes schizophrenia
enlarged ventricles
reduced grey matter
decreased temporal lobe volume
reduced limbic
neuropathology of schizophrenia
decreased presynaptic markers, oligodendroglia, thalamic neurones
typical vs atypical antipsychotics
typical- block D2 receptors. act on mesolimbic and mesocortical
atypical- block 5HT3, dissociate rapidly from D2. weight gain
nigrstriatal pathway
from substantia nigra pars compacta to the striatum
symptoms and cause catotonia
stupor, excitement, rigidity, wavy flexibility
caused by less GABA so less inhibition
tuberoinfundibular pathway
from arcuate and preventricular nuclei to infundibular region of hypothalamus
which is raised in schizophrenia
more mesolimibic, less mesocortical
structural changes schizophrenia
enlarged ventricles, decreased grey matter, decreased temporal lobe volume
where is serotonin produced
raphe nuclei
where is NA produced
locus corleus
treatment of
- acute mania
- acute bipolar depression
mania: antipsychotic plus mood stabilsier eg. lithium
depression: antidepressant with mood stabiliser cover
action astrocytes
• Provide structural support
• Nutritional support
o Convert glucose to lactate which they transfer to
neurones
• Reuptake of neurotransmitters
• Maintain ion concentrations in extracellular fluid
o Particularly potassium, which is released in large
quantities in highly active areas of brain
• Contribute to the blood brain barrier
o Induce expression of tight junctions between brain
what is immune privilege
There is constant surveillance of the CNS by immune cells, however
their activity is tightly regulated
▪ This tight regulation is essential since a strong inflammatory response
in the brain would leads to swelling and hence raised intracranial
pressure (bad)
3 types of NT and example
amino acids- GABA (GABAA/GABAB), glutamate (AMPA, NMDA), glyceine
biogenic amines- ACh, NA, DA, 5HT, H
Peptides- dynorphin, encephalin
where is serotonin and NA formed
5HT- raphe nuclei
NA- locus corleus
which disease causes by loss of ACh
Alzhimers
which disease caused by loss of DA
parkinsons
describe long term potentiation
• If the synapse is activated strongly, and a lot of glutamate is
released then additional AMPA receptors are inserted into the
postsynaptic membrane
• This is mediated by the entry of Ca through NMDA receptors
• Extra AMPA receptors means that the synapse will transmit
more readily (i.e. it ‘stronger’
• This is the process of long term potentiation (LTP) which is the
molecular basis for learning and memory
light green- lateral corticospinal tract
dark green- ventral corticospinal tract
purple- DCML
pink- STT- pain and temperature
peach- ventral STT- light touch
which lobe is hippocampus in
temporal
role cerebral peduncles and another name for them
connect cerebral hemispheres
- crus cerebri
Amaurosis fugax effects and cause
Amaurosis fugax is a temporary loss of vision in one or both eyes due to a lack of blood flow to the retina
central retinal artery occlusion
1st rank symptoms of schizophrenia
auditory hallucinations:
thought withdrawal, insertion and interruption.
thought broadcasting.
somatic hallucinations.
delusional perception.
feelings or actions experienced as made or influenced by external agents.
what does raphe nuclei form
serotonin
can thalamus damage affect movement
yes
what things are required for balance
- vision
- proprioception
- vestibular system
2/3 of these
what is internuclear opthalmoplegia?
ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron between two nuclei of cranial nerves (CN) VI and CN III
due to medial longitudinal fasiculus damage
what do photoreceptors synapse with
bipolar cells
how to determine if lesion is optic tract vs PVC
optic tract will show no macula sparing, PVC will
which pathway is responsible for loss of conjugate vision
medial longitudinal fasiculus
connects CN III, IV and VI
how can blockage of CA affect vision
compress third nerve nuclei which contains EDW and CNIII
are LMN affected by sharp cord transection between c3 c4
no, as they only exit at the level, not inbetween
where do spinal nerves exit?
cervical- above. eg. if c2/c3 cord transected, c3 would be affected
thoracic- exit below. if t2/t3 transected, t2 would be affected
action medial longitudinal fasiculus
- allows for conjugate movement
- inhibition of contralateral extraocular muscles
where does spinal cord terminate
L1/L2
how to increase reflexes
jendrassik manouver
where is SNc located
midbrain
what does rhombergs test show
sensory ataxia
patho sleep apnoe
not enough light reaching the brain
treatment sleep apnoea
postivie pressure mask, lose weight
role red nucleus
motor control
where do thalamoperforator branch from
PCA
where are cell bodies and dendrites located
grey matter
raphe nucleus forms…
serotonin/ 5HT3
raphe = 5HT3
anterior central sulcus
primary motor cortex
superior colliculus is in the …
midbrain
cerebellar artery also supplies the …
midbrain
internuclear ophalmoplegia is caused by damage to …
medial longitudinal fasiculus
tetorium cerebelli is at the level of the
midbrain
short term consequences of subarachnoid haemorrhage
- microthrombi occlude small distal arteries
- vasoconstriction from CSF irritant
- cerebral oedema
- sympathetic activation causing myocardial necrosis
long term consequence of subarachnoid haemorrhage
early rebreeding, acute hydrocephalus, global cerebral ischemia
