This document summarizes information about cerebrospinal fluid (CSF), including its physiology, production, absorption, circulation, factors affecting flow, and functions. It also discusses lumbar puncture (LP) procedures, indications, contraindications, and complications. Finally, it provides information on the analysis of CSF, mechanisms and signs/symptoms of increased intracranial pressure, types of brain herniation, mechanisms and types of brain edema, and idiopathic intracranial hypertension (IIH, also known as benign intracranial hypertension or pseudotumor cerebri).
This document summarizes information about cerebrospinal fluid (CSF), including its physiology, production, absorption, circulation, factors affecting flow, and functions. It also discusses lumbar puncture (LP) procedures, indications, contraindications, and complications. Finally, it provides information on the analysis of CSF, mechanisms and signs/symptoms of increased intracranial pressure, types of brain herniation, mechanisms and types of brain edema, and idiopathic intracranial hypertension (IIH, also known as benign intracranial hypertension or pseudotumor cerebri).
This document summarizes information about cerebrospinal fluid (CSF), including its physiology, production, absorption, circulation, factors affecting flow, and functions. It also discusses lumbar puncture (LP) procedures, indications, contraindications, and complications. Finally, it provides information on the analysis of CSF, mechanisms and signs/symptoms of increased intracranial pressure, types of brain herniation, mechanisms and types of brain edema, and idiopathic intracranial hypertension (IIH, also known as benign intracranial hypertension or pseudotumor cerebri).
This document summarizes information about cerebrospinal fluid (CSF), including its physiology, production, absorption, circulation, factors affecting flow, and functions. It also discusses lumbar puncture (LP) procedures, indications, contraindications, and complications. Finally, it provides information on the analysis of CSF, mechanisms and signs/symptoms of increased intracranial pressure, types of brain herniation, mechanisms and types of brain edema, and idiopathic intracranial hypertension (IIH, also known as benign intracranial hypertension or pseudotumor cerebri).
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 Severdementia, 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)