Skin

Subcutaneous

Connective tissue

Galae

Aponeurotica

Loose areolar connective tissue

Periosteum

                                      P.A.D.

Pia

Aarahnoid

Dura

Outer periosteal layer which is adherent to the inner surface of the skull.

Inner meningeal layer which is fused to the outer periosteal layer.

Falx cerebri a flat sheet of dura that is suspended from the roof of the cranium and separates the right and left cerebral hemispheres.

Tentorium cerebelli a tent-like sheet of dura that covers the upper surface of the cerebellum.

Portion of the intracranial cavity above and below the tentorium

***The tentorium cerebelli, together with the petrous portions of the temporal bones, divide the posterior fossa from the rest of the cranial vault***

Upper surface of tentorium --> occipital lobes and part of temporal lobes

Below --> Cerebellum

Epidural space - between the inner surface of the skull and the tightly adherent dura. Middle meningeal artery which enters the skull through the foramen spinosum and runs in the epidural space between the dura and the skull. Branch off the external carotid artery and supplies the dura.

Epidural hematomas

***Note: The middle cerebral artery is a branch of the internal carotid artery and supplies the brain.

Subdural space is located between the inner layer of dura and the loosely adherent arachnoid. Bridging veins traverse the subdural space. These veins drain the cerebral hemispheres and pass through the subdural space en route to the several large dural venous sinuses.

Subdural hematomas

Sigmoid sinuses --> internal jugular veins

Location of Frontal (anterior) horn of the lateral ventricles 

lateral foramina of Luschka

midline foramen of Magendie

ventral surface of the midbrain, between the cerebral peduncles.

***CN III

ventral to the pons

as they ascend from the pontomedullary junction along the clivus

***CN VI

          ***basilar artery

lumbar portions of the spinal column and contains cauda equina

***location where lumbar spinal tap is made

Genetic basis

Preceded by an aura or warning symptoms: visual blurring, shimmering, scintillating distortions, fortification scotoma (a characteristic region of visual loss bordering by zigzagging lines resemling the walls of a fort.

If pain is unilateral should get MRI to check for vascular malformation

Pain is often throbbing

Exacerbated by: light (photophobia), sound (phonophobia) or sudden head movement.

1:10 as common as migraine

Males 5:1

pain is extremely severe, often described as a steady, boring sensation behind one eye, 30-90 mins.

Unilateral autonomic symptoms

Inhaled O2 helps sometimes

steady dull ache (bandlike sensation)

some patients have tension-type headaches that occur continuously every day for years.

commonly associated with psychological stress (also commonly seen in posttraumatic headache)

increase in intracranial pressure

worse when laying down during the night

headache and elevated intracranial pressure with no mass lesion.

Adolescent females.

Acetazolamide.

Shunting procedures

treatable cause of headache

old people

vasculitis affects temporal arteries and those supplying the eye

must measure erythrocyte sedimentation rate (ESR) and biopsy of temporal artery

need to treat with steroids to prevent possible vision loss.

1. Compression and destruction of adjacent regions of the brain can cause neurologic abnormalities.
2. A mass located within the cranial vault can raise the intracranial pressure, which causes certain characteristic symptoms and signs.
3. Mass lesions can displace nervous system structures so severely that they are shifted from one compartment into another (herniation).

Autoregulation

CPP = MAP - ICP

CPP --> Cerebral perfusion pressure

MAP --> Mean arterial pressure

ICP --> Intracranial pressure

- Headache (worse in the morning)

- Altered mental status (irritability and depressed level of altertness and attention) ***most important

- Nausea and vomiting (suddenly without much nausea projectile vomiting)

- Papilledema (engorgement and elevation of the optic disc) leads to blurring or visual loss (most commonly increased blind spot or concentric visual field deficit) or diplopia (downward traction on CN VI)

- Cushing triad --> hypertension, bradycardia, and irregular respirations

Herniation of the medial temporal lobe especially the uncus inferiorly through the tentorial notch.

Clinical triad of a "blown" pupil, hemiplegia, and coma. Compression of oculomotor nerve CNIII usually ipsilateral to the lesion.

unresponsive pupil (blown) --> later impairment of movement

Compression of cerebral peduncles can cause hemiplegia contralateral (corticospinal tract --> pyramidal decussation)

***Note: If it's bad it'll be ipsilateral Krnohan's phenomenon

Location: Tight potential space between the dura and the skull

Usual cause: Rupture of the MMA due to fracture of the temporal bone by head trauma.

Clinical features and radiological appearance: Rapidly expanding hemorrhage under arterial pressure peels the dura away from the inner surface of the skull, forming a len-shaped biconvex hematoma does not spread past the cranial sutures. Lucid interval.

Location: Potential space between the dura and the loosely adherent arachnoid.

Usual cause: Rupture of the bridging veins, shear injury as they cross from the arachnoid into the dura.

Clinical features: Large area and forming a crescent-shaped hematoma.

- old people

- bridging veins

- no trauma sometimes

- weeks to months

- headache, cognitive impairment, and unsteady gait

- focal dysfunction of the underlying cortex may result in focal neurologic deficits

- occasionally, focal seizures

For a significant subdural hematoma to immediately after an injury, the impact velocity must be quite high.

Radiological appearance: crescent shape spreaqd over a large area. Hyperdense --> isodense --> hypodense

Hematocrit effect for mixed density with denser acture blood settling to the bottom.

Location: CSF-filled space between the araqchnoid and the pia, which contains the major blood vessel of the brain.

Radiological appearance: blood can be seen on CT to track down into the sulci following the contours of the pia.

Usual cause: spontaneous and traumatic

Patients "worst headache of my life" feeling like head is suddenly about to explode.

Happens as a result of rupture of an arterial aneurysm in subarachnoid space.

Note: look for atherosclerotic disease and marfan's syndrome

saccular aneurisms or berry aneurysms

typically have a neck connected to dome that can rupture

AComm --> 30% (most common)

Pcomm aneurysm (25%) from internal carotid --> painful third-nerve palsy

CT scan without contrast because both subarachnoid blood and contrast material appear white on the scan. Would make it tough to see small hemorrhages.

Lumbar puncture --> yes for subarachnoid hemorrhage with negative CT but not positive CT b/c of increased transmural pressure across the aneurysm can occasionally precipitate rebleeding

Angiogram --> exact location and size of aneurysm

"triple H" therapy inducing:

- hypertension

- hypervolemia

- hemodilution

in the intensive care unit after aneurysm has been clipped or coiled

Bleeding into the CSF from damaged blood vessels associated with cerebral contusions.

Vasospasm is not usually seen.

Location: Within the brain parenchyma in the cerebral hemispheres, brain-stem, cerebellum, or spinal cord.

Cause: Trauma

Contusions most common at temporal and frontal poles

Least common occipital poles

Side of impact --> coup injury

opposite of impact --> contrecoup injury

Combination of hemorrhage location layers

intraparenchymal hemorrhage --> hypertensive hemorrhage

Most to least common location --> basal ganglia (putamen), thalamus, cerebellum, and pons

peak of symptoms 3 days

from actual blood vessels --> intraventricular extension

from actual ventricles --> intraventricular hemorrhage

Low rebleed rate. Gradual surrounding edema.

- seen in older patients

- occipital, parietal, temporal, or frontal lobe.

- most common cause --> amyloid (congophilic) angiopathy

1. Arteriovenous malformations
2. Cavernomas (also called cavernous hemangiomas, cavernous angiomas, or cavernous malformations)
3. Capillary telangiectasias (capillary angiomas)
4. Developmental venous anomalies (venous angiomas, venous malformations)

abnormal dilated vascular cavities lined by only one layer of vascular endothelium. Not visible on angiograph but is with MRI (dark rim on T2)

- head trauma

- Battle's sign / "raccoon eyes"

- between external periosteum and galea aponeurotic --> "goose egg" or subgaleal hemorrhage

Newborns --> between skull and external periosteum (pericranium) during delivery cephalohematoma

1. excess CSF production (rare)
2. obstruction of flow at any point in the ventricles or subarachnoid space (most common)
3. decrease in reabsorption via arachnoid granulations

- foramen of Monro (laterals & third)

- cerebral aqueduct (third & fourth)

- fourth ventricle (fourth & spinal column)

Causes hydrocephaalus when the arachnoid granulations are damaged or clogged.

***difficult to distinguish clinically from obstruction of CSF flow both have similar causes

1. Communicating hydrocephalus is caused by impaired CSF reabsorption in the arachnoid granulations, obstruction of flow in the subarachnoid space, or rarely by excess CSF production.
2. Noncommunicating hydrocephalus is caused by obstruction of flow within the ventricular system.

-old people

- gait difficulties

- urinary incontinence

- mental decline

- Headache

- Lethargy

- photophobia & phonophobia

- Fever

- Nuchal rigidity (stiff neck): unable to touch chin to chest

- Kernig's sign: pain in hamstrings when knees are straightened

- Brudzinski's sign: flexed neck --> flexed hips

Note: Check out the CSF for diagnosis only after head CT

CSF Profile

high WBC (polymorphonuclear)

high protein

low glucose

less fulminant than bacterial meningitis.

CSF profile

-high WBC (lymphocytes)

 - normal or mildly elevated protein

- normal glucose

viral infection of the brain parenchyma usually involving the meninges resulting in meningoencephalitis. Most common cause herpes simplex virus type 1.

CSF profile:

high WBC (lymphocytic)

high protein

normal to reduced glucose

common parasitic infection of HIV patients and most common cause of intracranial mass lesions

MRI --> ring-enhancing lesions (dark center on T1)

Note: primary central nervous system (B cell lymphoma) looks very similar and is 2nd most common cause of IML in HIV patients. Do biopsy.

subcutaneous tissue --> ligaments of the spinal column --> dura --> arachnoid --> CSF in subarachnoid space of the lumbar cistern

Note: CSF of lumbar cistern in direct communication with CSF in the ventricles and flowing over the surface of the brain

subarachnoid hemorrhage, hemorrhaic herpes encephalitis, traumatic tap.

1. number of RBCs usually decreases from the first to last CSF tube collected in a traumatic tap, not subarachnoid hemorrhage
2. CSF is centrifuged (xanthochromic = hemorrhage)