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Increased ICP: A) Headache

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The key takeaways are that CSF is produced and absorbed continuously, its flow is affected by pulsations of arteries and movement of ependymal cells, and it serves to provide support and a stable environment for neurons.

The factors that affect CSF flow are pulsations of cerebral and spinal arteries in the subarachnoid space, movement of cilia of ependymal cells, and the continuous production and absorption of CSF which creates positive and negative pressures.

The causes of increased intracranial pressure include cerebral or extracerebral masses, generalized brain swelling, increased venous pressure, obstruction of CSF flow or absorption, and increased CSF volume from conditions such as subarachnoid hemorrhage or meningitis.

CSF

Physio Vol 120 ml


Rate of formation: 0.35ml/ min = 21-22 ml/hour = 500 ml/ day.
CSF renewed 4-5 times daily.
Secret Choroid plexus ventricles
Absorp Arachnoid villi in venous sinuses (mainly SSS)
Spinal nerve pockets into lymphatic system.
Gap junctions () ependymal cells & () pial cells → into brain extracellular space.
Small vein in SAS → venous blood
Circ Lat vent→ Monro → 3rd → cerebral aqueduct of sylvius → 4th →foramen of Lushka,
Magendi → SAS
Factors Pulsations of cerebral, spinal arteries in SAS.
Affect Movement of cilia of ependymal cells.
flow + ve and -ve pressure created by continuous production and absorption.
Funct support, stable env for neurons, transporter metabolites
LP Proced Lt lat, flexed hip, knee, L345, lignocaine local anasth, needle 22G
Indicat D: Infection (3), SAH (xanthochromia), Ms (OCB), Mg, sarcoidosis, vasculitis, IIH
Th: ↓CSF pressure, contrast media, spinal anasth
CI IC SOL, local skin infect, anticoagulant, coagulation defect, spinal block
Comp 1) Headache after few hr→ throbbing, associated with
N, V, giddiness, pain in the neck & back.
2) Diplopia due to transient uni or bilateral 6th nerve palsy.
3) S.A. bleeding disorder, throbbing pain.
4) Introduction of leukaemic cells or microorganisms into SAS, prolapsed
intervertebral disc.
Analysis Normal, infection (3), SAH, MS
Increased ICP
Mech 1)Cerebral/extracerebral mass: tumor, infarction, contusion, abscess
2)Generalized brain swelling: Anoxia, HTN, Encephalopathy, trauma, acute liver failure
3)venous pressure: HF, SVC obst, mediastinal syndrome, cerebral venous thrombosis
4)Obstruction of CSF flow or absorption: hydrocephalus
5)CSF volume: SAH, meningitis, production (choroid plexus tumor)
C/P A)Headache:
 D2 distortion of pain sensitive structures (dura & blood vessels)
 Throbbing, ↑in the morning,
 Frontal or occipital or both, may be unilateral
 ↑by exertion, cough, straining, sudden postural change.
B)Vomiting:
More in the morning with headache (d2 compression or ischemia of vomiting center in medulla)
C)Papilloedema:
 D2 to CSF pressure in optic nerve sheath→ prevent venous drainage, axoplasmic flow in
optic neurons) → not cause neuronal damage with maintenance of CBF.
D)Bradycardia: D2 cardiac center dysfunction or Tachycardia in infratentorial lesions
E)Breathing control:
 Sudden ICP slow deep resp
 Late, chyne stokes, shallow rapid in deep coma
F)False localizing signs
 Uni or bilateral 6th , bilateral extensor planter, grasp reflex, 3rd N palsy
Brain Herniation
Uncal Unilateral expanding mass → tentorial PCA occluded→ HH, (BS infarct)
(tentorial lateral) (uncal) herniation as the medial edge of RF →conscious level.
temporal lobe herniates through the tentorial Pressure on opposite cerebral
hiatus peduncle (Kernhan's notch) → ∆ limb
e Continuous ↑ICP→ central herniation weak on same side of lesion (false
locating sign).
Compression 3rd → pupil dilatation,
failure to react to light.
Central Midline lesion or diffuse swelling of cerebral Pressure on dorsal aspect
(tentorial hemispheres → ventral displace of midbrain , (pretectum, superior colliculi) →
central) diencephalon through tentorial hiatus → impairs eye movements → upward
damage of these structures by mechanical gaze is initially lost.
distortion , ischemia 2ry to stretching of Diencephalon, midbrain damage
perforating vessels → conscious level
May progress to tonsillar herniation. Pupil→ initially small →
moderately dilated and fixed to light.
Downward traction on pituitary
stalk, hypothalamus → D.I.
Subfalcine Occur early as SOL→ angulate gyrus under Seldom produces any clinical effect.
Cingulate falx Ipsilateral ACA occlusion.
(midline shift)
Trans-calvarial Brain, #, surgical site
Tonsillar Subtentorial expanding mass → herniation of Tonsillar impaction in foramen
(↓cerebellar) cerebellar tonsils through foramen magnum + magnum → neck stiffness, head tilt.
3 Chiari malf A degree of upward herniation through Brain stem pressure :
tentorial hiatus a) Conscious level.
- Clinical picture difficult to differential b) Resp irregularities; chyne
diagnosed from direct brain stem strokes, central
compression. hyperventilation, ataxic,
gasping, arrest.
Reversed Cerebellum, tentorium Push MB up
tentorial
(↑cerebellar)
Brain edema
Vasogenic (Open barrier) Cytotoxic (Cellular) Interstitial
Path Cap permeability & open Disruption of cell memb Block CSF brain fluids
BBB cellular swelling
AE Tumor Hypoxia with IC osmoles Obstructive
Abscess (Na, H, lactate) hydrocephalus
Hge, infarction, contusion Acute hypoosmolatity Pseudotumor cerebri
Acute demyelination (SIADH)
Purulent meningitis Dysequilibrium synd
Site Mainly white matter Grey> white Periventricular white matter
Path Open BBB Intact BBB Intact BBB
↑cap permeability Disruptn cell memb → cell swell Block CSF → ↑brain fluid
MRI Contrast enhancement No enhancement CT: perivent hypodensity
↑diffusion coefficient ↓ diffusion coefficient
CSF protein Normal protein
C/P Focal deficit, consc, ICP consc, myoclonus, seizures Severdementia, gait dist
TTT Steroid: in tumor, abscess Steroid: not effective Steroid: uncertain role
Osmotherapy Osmotherapy Osmotherapy: rarely used
Treatment of brain edema:
1) Treatment of the cause
2) Care of comatose patient
3) Pharmacological ttt:
 Corticosteroid: in vasogenic edemad2 tumor, ICH, head trauma, meningitis (4mg/6hr)
 Osmotherapy (mannitol)
 Drugs CSF formation: actozolamide
4) Others: hyperventilation, hypothermia, barbiturate ttt

IIH = BIH = PseudoTm cerebri


Def Persistent ↑CSF pressure in absence SOL é ventricles N or ↓size
Incid ♀, 3rd-4th decade
AE: Idiopathic
Arachnoid grandulation: d2 previous inflam, SAH
Obstruction of venous drainage: d2 DST, hypercoagulable state
Endocrine Preg, menarch, menst irreg, Addison, acromegaly, ↓thyroid, ↓PTG
Diet Obesity, ↑vitA
Drug OCP, steroid édrawal, amiodarone, danazole, tetracycline, nitrofurantoin
Hematoloic IDA, Polycythemia rubra vera
Others SLE, meningism é systemic infection, polyneuritis, empty sella syndrome
Path ↑CSF formation
↓CSF absorption
↑Venous pressure from ↑I.Abd.P
Abn cerebral microvasculature é ↑water content brain (sort of brain edema)
Symp Headache:
Diffuse, but may be bitemporal or bioccipital
Constant, severe > any previous H/A,
↑at night, on awakening, by cough, straining, ↓by tapping
Vomiting (occasional)
Transient visual obscuration:
D2 intermittent ischemia optic disc
Uni or bilateral
Brief episodes (seconds) of greying, blackening
by change in posture or valsalva maneuver, by tap & medical ttt
Ocular: ↓VA, diplopia,
Self-audible bruit in ears (pressure diff in cranial, jug V)
Signs Papilledema
6th, 3rd CN palsy
Field defect: enlarged blind spot, central/centrocecal periph field constriction
DD Other causes papilledema
Inv CT, MRI: small, slit like vent, no shift (exclude SOL, DST)
LP: after exclusion SOL, coagulation profile, opening pressure >250mmH2O
Visual field (perimetry)
TTT Medical ↓Wt, Analgesics H/A, Avoid causative drugs
CAI (acetazolamide 1-4gm/d),
Diuretic (Lasix 40-160mg/d),
Osmotic agent: Glycerol ¼-½ml/kg/4-6hr, mannitol
Steroid not used d2 rec papilledema after édrawal, ↑wt (used for short course)
LP Series of CSF édrawal (15-30ml)
Surgic Indication: failed medical ttt, threatened vision
Types: ventriculoperit shunt, optic sheath fenestration, subtemporal decompression
HCP
Def ↑CSF vol éin skull d2 abnormal production, circulation, absorption
AE Obstructive Communicating
Intravent: obst MSLM ↑CSF production: ch plexus papilloma
Extravent: obst base brain, tentorial level
Congenital: Arnold chiari, IU infection Impaired CSF absorption:
Post-inflam: TB, M, carcinomatous M Congenital: arach villi agenesis
Post-Hge: SAH, IVH ↑CSF Pr (SC Tm, polyneuritis)
Mass lesion: SOL, ICH, Cerebellar hge, infarct Tm seeding (ependymoma)
Venous insufficiency (Sinus thrombosis)
CP Before closure fontanells After closure fontanels
↑ICT (mild, late) ↑ICT: 3B
Skull: ↑head circumf all diameter> 75cm Skull: No enlargement if >3yr
F&O bossing, craniofacial disproportion Venous congestion scalp
Sun setting eye Cracked pot
Wide suture, enlarged ant fontanel
Cracked pot on percussion
M: weakness, wasting, spasticity LL>UL M: clumsiness, no gross weakness
↑Rx, ext planter ↨Rx, ext planter
S: intact S: intact
CN: optic atrophy, rarely papilledema, ↓VA CN: 5, 6, 7
Squint, sluggish pup Rx,
Loss upward, lateral gaze
↓Cognition, memory, N IQ (in mild cases) Giddiness, Mild MR
Convulsions (common) Convulsions (↓)
Obesity, DI (hypoth, pit) Obesity, genital atrophy (pit)
CSF rhinorrhea (rare) Otitic HCP:
Bobble head doll synd:  Purulent ear disch,
2-4 oscillation of head movement with  Ipsilateral 6th N palsy
psychomotor retardation  Papilledema
rd
D2 obst in or near 3 vent or aquiduct
Inv Skull transillumination
Skull US: follow up infant for progressive HCP (supependymal & IVH)
Skull measurement: for follow up
Skull X-ray: clavarium, suture diastasis, thinning of convolutional markings, eroded clinoid
process, deepened sella turcica
CT, MRI
Pressure monitoring LP: CSF pulse wave analysis is more reliable
TTT Medical Limited value (acetazolamide, lasix)
Surgical TTT AE (excision ch plexus)
Obstructive: ventricular drain, ventriculoperit shunt, ventriculostomy
Communicating: LP, lumboperitoneal shunt
NPH (Adam Hakim)
AE CP ∆ Inv
SAH Gait apraxia CT: enlarged ventricle, dilated T horn
Post-M Subcortical dementia MRI: measure vol ventric/SAS CSF
Achondroplasia Urgency, frequency, incontinence CSF flowmetry, No WM changes
Mucopolysaccharoidosis LP: continous IC monitoring
of meninges (if B wave >5% → need drainage operat)

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