Neuropathophysiology

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Explain how disturbance in ICP-volume relationships can give rise to raised ICP.: ICP is determined by:
1)volume of brain parenchyma
2)blood volume
3)CSF volume

Since skull is noncompressible, an increase in any of the three will lead to a compensatory reduction or shift of other components.

As ICP increases (in order):
1)CSF is 1st displasced thru foramen magnum
2) blood displaced from intracranial to extracranial venous system
3) shift and herniation of brain contents

When capacity to compensate for increased volume and pressure is exceeded, inc ICP results!
Why is increased ICP deleterious?: 1)Inc ICP affects cerebral perfusion:
CPP=MAP-ICP (normal CPP=70-120mmHg)

Cerebral autoregulation maintains CPP in normal range regardless of BP--
BUT autoreg can fail in dz states

As ICP inc, CPP dec & ischemia can result. MAP will often reflexively inc.--> cerebral edema & worsening ICP

2) Inc. ICP can lead to herniation of brain contents
What are the normal values of: CPP ICP brain volume CSF volume CSF synthesis rate: CPP=70-120mm H20

ICP=60-200mm H20

Average brain volume=1400mL

CSF volume=150mL (75mL w/in intraventricular system)

CSF synthesis rate by choroid plexus= 450-500mL per day (20mL/hr)
What are the non-specific clinical features of increased ICP?: headache
nausea/vomiting
decreased LOC

papilledema
Bilateral VI nerve palsy
(diplopia, esotropia->cross-eyed)
Name the 3 general categories of cerebral edema, the underlying mechanisms, and the list of common causes of each?: VASOGENIC EDEMA:
Â• MECH= Failure of BBB leading to extravasation of plasma.
Â• CAUSES= tumor, abscess, infarct, meningitis, lead encepalopathy

CYTOTOXIC EDEMA:
Â• MECH=Metabolic failure of cell membrane function leading to intracellular Na+ accumulation and osmotic neuronal swelling
Â• CAUSES=Hypoxia, ischemia, hypo-osmolar states, meningitis, hepatic encephalopathy

INTERSTITIAL (hydrocephalic) EDEMA:
Â• MECH=Seepage of ventricular fluid thru ependyma into periventricular white matter
Â• CAUSES=obstructive & nonobstructive hydrocephalus
For Subfalcine herniation, name the: 1)ANATOMICAL STRUCTURES INVOLVED 2)CLINICAL MANIFESTATIONS: SUBFALCINE:
1)Herniation of cingulate gyrus beneath falx cerebri
2)Could lead to occlusion of ACA resulting in medial frontal infarct and leg paralysis
For uncal/transtentorial herniation, name the: 1) Anatomical structures 2) clinical manifestations: UNCAL/TRANSTENTORIAL:
1)Herniation of uncus of temporal lobe down through tentorial hiatus
Â•compression of ipsilat 3rd nerve
Â•compression of Ipsilat +/- contralat cerebral peduncles against tentorium
Â•midbrain (Duret) hemorrhages
Â•PCA compression

2)Ipsilat pupil dilated and fixed
Â•ipsilat eye down and out
Â•contra UMN signs due to ipsi peduncle compression
Â•ipsi UMN signs as contra cerebral peduncle compressed against tentorial edge
Â•dec consciousness
Â•contra(or sometimes bilat)visual field defects from PCA infarcts.
For Tonsillar herniation, name the: 1)ANATOMICAL STRUCTURES INVOLVED 2)CLINICAL MANIFESTATIONS: 1)Herniation of cerebellar tonsils through foramen magnum compressing descending motor tracts, and cardiorespiratory centers in medulla

2)Bilateral UMN findings, subsequently decorticate then decerebrate posturing; coma; cardiorespiratory compromise
Explain anatomically & physiologically how progressive increased ICP can lead to death.: Expanding mass lesion in middle cranial fossa can result in uncal herniation then progressive rostrocaudal brainstem compression and finally tonsillar herniation.

The course will be as follows:
1.Decrease in alertness (reticular activating system)
2.Dilatation and lack of responsiveness of the ipsilateral pupil (IIIrd nerve compression by the herniating uncus).
3.Usual contra hemiparesis caused by the underlying lesion and/or compression of ipsilateral cerebral peduncle will worsen
4. Ipsilat hemiparesis may develop as the opposite cerebral peduncle is forced against the edge of the tentorium.
5.Cheyne-Stokes respiration (alternating periods of apnea and hyperpnea, typically in 1 min cycles)
6.As the midbrain becomes compressed, both PS and sym systems affected bilat, and pupils become mid-size and unreactive.
7. As the pons and medulla become compressed, other brainstem reflexes become lost and bilateral upper motor neuron findings develop with eventual decerebrate rigidity.
8.Respiratory patterns deteriorate and eventually cardiorespiratory arrest occurs as tonsillar herniation develops.

**In addition to the mechanism described above, tonsillar herniation can result from a mass lesion arising in the infratentorial compartment (posterior fossa), such as a hematoma in the cerebellum, a cerebellar abscess or a neoplasm.
What are the pathophysiological mechanisms underlying cerebral ischemia and infarction?: normal cerebral blood flow will remain constant (50mL/100gm/min) even if BP or intracranial pressure changes because of autoregulation of vascular resisitance
Distinguish coup and countrecoup injury and explain the mechanisms underlying these injuries: Both caused by blunt injury to the brain.

COUP injuries refer to injuries located directly at the point of impact in an acceleration or deceleration injury. **Coup injuries tend to be more conspicuous in acceleration injury.

CONTRECOUP injuries are located opposite (180 degrees from) the point of impact. **often more extensive than coup injuries, especially when the point of impact is located in the posterior head regions.
**Contrecoup injury is more prominent in deceleration injury.
Know the two general categories of hydrocephalus.: COMMUNICATING-
obstruction to CSF flow in subarachnoid space or impaired resorption of CSF at the level of the arachnoid granulations.

NON-COMMUNICATING=
obstruction of the normal flow of CSF through the ventricular system.
List the sites where ventricular obstruction can occur and the most common causes at these sites.: COMMUNICATING=
1. Meningitis (acute or chronic) (bacterial, fungal or neoplastic)
2. Subarachnoid hemorrhage

NON-COMMUNICATING=
*Lateral Ventricle or Foramen of Munro
1. ST tumor
2. IV hemorrhage
3. Ventriculitis

*3rd Ventricle
1. Thalamic, hypothalamic or suprasellar pituitary tumor
2. Colloid cyst

*Aqueduct of Sylvius
1. Congenital aqueductal stenosis or atresia (anoxic or infectious)
2. Vein of Galen aneurysm
3. Ventriculitis
4. Brainstem tumor

*4th Ventricle or Foramina of Luschka and Magendie
1. Cerebellar Tumors
2. 4th ventricular ependymoma
3. Chiari malformation
4. Dandy Walker malformation
5. Cerebellar hematoma (or infarct)
Know the pathogenesis, radiologic appearance and clinical features of epidural hematomas.: PATHOGENESIS:
Lies within the epidural space between the inner table of the skull and dura.
Secondary to laceration middle meningeal artery from a depressed fracture of the temporal or parietal bone.
*Usually ipsilateral to side of impact.
*Usually due to arterial bleeding, so rapidly accumulate

CLINICAL:
Rapidly progressive focal signs and depressed LOC within hours
**often have a short "lucid interval" after trauma

RADIOLOGY:
Lens-shaped or convex area of increased attenuation (or radioopaqueness) beneath the inner table of the skull on unenhancd CT.
**Due to the attachment of the dura, epidural hematomas do not cross the midline.
Know the pathogenesis, radiologic appearance and clinical features of subdural hematomas.: PATHOGENESIS:
Located in the subdural space b/t dura mater and arachnoid membrane.
*Due to venous bleeding from rupture of tiny cerebral bridging veins tethered between the cortex and venous sinuses.
*More common in the elderly population because age-related cerebral atrophy increases the distance between the brain and venous sinuses, making the cerebral veins more prone to rupture in acc-dec injury.

CLINICAL:
*Present as subacute to chronic
*Can have progressive confusion and drowsiness, sometimes with headache.

RADIOLOGY:
crescentic or concave shape on unenhanced CT scans.
Be aware of the basic characteristics of skull fractures and other forms of head injury.: PENETRATING INJURIES:
Intracranial hemorrhage, cerebral laceration and edema
**Missile injuries cause more damage than can be accounted for by the size of the missile b/c it quickly expands causing an explosive effect. (Missiles can also ricochet in the skull leading to further damage)
**Infections frequently complicate penetrating injuries to the head. Seizures are a common sequela in survivors.

CONCUSSION
Transient loss of consciousness without pathological alteration of the brain. The pathophysiological substrate of concussion is not known.

DIFFUSE AXONAL INJURY:
Shearing forces can rupture axons and cause severe neurologic deficits w/ no visible gross brain damage.

INTRAPARENCHYMAL HEMORRHAGE:
From depressed skull fractures and contusion with cerebral edema.

DISSECTION OF CAROTID ARTERY:
From flexion-extension neck injuries, leading to cerebral infarction.
**Carotid dissection should be considered in any trauma case with hemiplegia where CT scans fails to show subdural/epidural bleeding or contusion.
Outline therapeutic approaches to raised ICP caused by trauma.: To decrease ICP:
1.Remove CSF by:
- placing a tube in the ventricles that drains CSF into a closed system outside the patient. This is limited by the volume of ventricular CSF, which is often reduced in trauma, and the rate of CSF production which is slow (20 ml/hr).

2.Decrease the intravascular volume. If the patient is hyperventilated, the dec CO2 concentration in the blood will cause vasoconstriction. Unfortunately, this only works until brain adjusts to the change in pH, perhaps a day at most.

3. Decrease the volume of edema. If an osmotically active compound that does not cross the BBB is given by IV, osmotic pressure will draw water out of the brain. The compound most often used is MANNITOL. Unfortunate properties of mannitol include its diuretic properties, leading to a loss of intravascular volume and hypotension. In addition, there is good evidence that mannitol will enter areas of traumatic edema, as the blood brain barrier is disrupted in areas of damaged brain. This will draw water into the brain over time!

The neurosurgeon uses all of these methods to try to control ICP in the setting of traumatic brain injury, but careful monitoring is required. In addition, BP is maintained at a high normal level, with a goal of keeping CPP above 50 to 60 mmHg.
Outline therapeutic approaches to raised intracranial pressure caused by hydrocephalus: Get CSF to a location where it can be absorbed.
Emergently, an external drain can be placed, but ultimately either the block in CSF prod must be bypassed or the CSF delivered to a location where is can be absorbed.
*Bypassing the block is usually done endoscopically.
- If the block is at on foramen of Munro, it can be bypassed by fenestration of the septum pellucidum.
- If the block is at the aqueduct of Sylvius, it can be bypassed by fenestrating the floor of the third ventricle.

Shunting: A small tube that drains CSF from the ventricles to the peritoneal cavity (ventriculo-peritoneal shunt), the right atrium (ventriculo-atrial shunt), or the pleural cavity (ventriculo-pleural shunt).
What does the ACA supply and what are symptoms if it is occluded?: ACA supplies medial surface and superior border of frontal and parietal lobes

Sx=paralysis of contralateral leg
What does the Internal Carotid supply and what are symptoms if it is occluded?: supplies the retina via the opthalmic artery as well as the ACA and MCA areas of the brain.

Sx depend on collateral flow. Can have no sx with occlusion or infarct in MCA and/or ACA.
If an embolus from the CCA or ICA to the opthalmic artery, can have transient monocular blindness (amaurosis fugax)
What does the MCA supply and what are symptoms if it is occluded?: Lateral surface and deep structures of frontal and parietal lobes & superolateral portion of temporal lobe.

SX= contralat paralysis of lower face
paralysis of contralat arm
weaknes of contralat leg
contralat sensory dysfunction
contralat homonymous hemianopsia
aphasia (dominant hemisphere)
constructional apraxia (non-dominant hemisphere)
What does the MCA penetrator/ Thalamoperforant supply and what are symptoms if it is occluded?: supplies internal capsule and basal ganglia

Sx of int capsule infarction= contralat pure motor hemiparesis
What does the PCA supply and what are symptoms if it is occluded?: supplies occipital loves and inferomedial parts of temporal lobes

Sx=contralateral homonymous hemianopsia
What does the PCA penetrator/ Thalamoperforant supply and what are symptoms if it is occluded?: supplies thalamus

sx=contralateral sensory loss, often painful
What does the vertebral artery supply and what are symptoms if it is occluded?: supplies medulla and part of the cerebellum through short or longer branches.

Sx=infarct of medulla and/or cerebellum causes
lateral medullary syndrome with ipsilateral ataxia, ipsilateral sensory disturbance of face and contralat sensory disturbance of arm+ leg
What does the Basilar artery supply and what are symptoms if it is occluded?: midbrain & parts of cerebellum thru shorter or longer branches. Short penetrating paramedian branches supply the base of the pons containing the corticospinal fibers

Sx=quadriplegia, bilateral facial paralysis, inability to swallow or speak "LOCKED-IN SYNDROME"
What are the four major pathophys mechanisms underlying cerebral ischemia and infarction?: 1) Thrombosis
2) embolism
3) low flow states
4) vasospasm
THROMBOSIS Vessel wall disorders: 1) ATHEROMA
ANTERIOR CIRC: common extracranially near bifurcation of CCA or in proximal ICA

Also common intracranial in siphon loop of ICA or in proximal MCA or ACA

POSTERIOR CIRC:
common extranially near origin of vertebral arteries (often asymptomatic)

Also intrancranially in the distal vertebral or basilar arteries. (or proximal PCA)

2) Hypertensive small vessel Dz:
HTN predisposes to atheroma-->get small changes in walls of deep penetrating arterioles (lipohyalinosis)
Vessels can occlude, causing small infacrts (lacunes)
**lenticulostriate branches of MCA supplying int. capsule are most affected

vasculitis of cerebral vessels predisposes to thrombosis. Can be infectious (ex-meningitis) or

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