The brain is shielded by the cranial vault (hair, skin, bone, meninges, and cerebrospinal fluid [CSF]), which intercepts the force of a physical blow. Below a certain level of force (the absorption capacity), the cranial vault prevents energy from affecting the brain. The degree of traumatic head injury usually is proportional to the amount of force reaching the cranial tissues. Furthermore, unless ruled out, neck injuries should be presumed present in patients with traumatic head injury.

In acceleration-deceleration cervical injuries, the head is propelled in a forward and downward motion in hyperflexion. A wedge-shaped deformity of the bone may be created if the anterior portions of the vertebrae are crushed. Intervertebral disks may be damaged; they may bulge or rupture, irritating spinal nerves. Then the head is forced backward. A tear in the anterior ligament may pull pieces of bone from cervical vertebrae. Spinous processes of the vertebrae may be fractured. Intervertebral disks may be compressed posteriorly and torn anteriorly. Vertebral arteries may be stretched, pinched, or torn, causing reduced blood flow to the brain. Nerves of the cervical sympathetic chain may also be injured.

A complex arrangement of ligaments holds the vertebrae in place. Some of the ligaments are barely a centimeter long, and all are only a few millimeters thick. In a whiplash injury, ligaments may be badly stretched, partially torn, or completely ruptured (arrows). Injuries of neck muscles may range from minor strains and microhemorrhages to severe tears. The anterior longitudinal ligament, running vertically along the anterior surface of the vertebrae, may be injured during hyperextension. The posterior longitudinal ligament, running on the posterior surface of the vertebral bodies, may be injured in hyperflexion. The broad ligamentum nuchae may also be stretched or torn.

Closed trauma is typically caused by a sudden accelerationdeceleration or coup/contrecoup injury. In coup/contrecoup, the head hits a relatively stationary object, injuring cranial tissues near the point of impact (coup); then the remaining force pushes the brain against the opposite side of the skull, causing a second impact and injury (contrecoup). Contusions and lacerations may also occur during contrecoup as the brain’s soft tissues slide over the rough bone of the cranial cavity. In addition, rotational shear forces on the cerebrum may damage the upper midbrain and areas of the frontal, temporal, and occipital lobes.

The brain of a patient with Alzheimer’s disease has three characteristic features: neurofibrillary tangles (fibrous proteins), neuritic plaques (composed of degenerating axons and dendrites), and neuronal loss (degeneration).

Neurofibrillary tangles are bundles of filaments found inside neurons that abnormally twist around one another. Abnormally phosphorylated tau proteins accumulate in the neurons as characteristic tangles and ultimately cause neuronal death. In a healthy brain, tau provides structural support for neurons, but in patients with Alzheimer’s disease, this structural support collapses.

Neuritic plaques (senile plaques) form outside the neurons in the adjacent brain tissue. Plaques contain a core of beta-amyloid protein surrounded by abnormal nerve endings or neurites. Overproduction or decreased metabolism of betaamyloid peptide leads to a toxic state causing degeneration of neuronal processes, neuritic plaque formation, and eventually neuronal loss and clinical dementia.

Tangles and plaques cause neurons in the brain of the patient with Alzheimer’s disease to shrink and eventually die, first in the memory and language centers and finally throughout the entire brain. This widespread neuron degeneration leaves gaps in the brain’s messaging network that may interfere with communication between cells, causing some of the symptoms of Alzheimer’s disease.

Current research suggests an excess accumulation of glutamate (an excitatory neurotransmitter) in the synaptic cleft. The affected motor units are no longer innervated, and progressive degeneration of axons causes loss of myelin. Some nearby motor nerves may sprout axons in an attempt to maintain function, but, ultimately, nonfunctional scar tissue replaces normal neuronal tissue.

AVMs lack the typical structural characteristics of the blood vessels. The vessel walls of an AVM are very thin; one or more arteries feed into the AVM, causing it to appear dilated and torturous. The typically high-pressured arterial flow moves into the venous system through the connecting channels to increase venous pressure, engorging and dilating the venous structures. An aneurysm may develop. If the AVM is large enough, the shunting can deprive the surrounding tissue of adequate blood flow. Additionally, the thin-walled vessels may ooze small amounts of blood or actually rupture, causing hemorrhage into the brain or subarachnoid space.

Bell’s palsy reflects an inflammatory reaction around the seventh cranial nerve, usually at the internal auditory meatus where the nerve leaves bony tissue. The characteristic unilateral or bilateral facial weakness results from the lack of appropriate neural stimulation to the muscle by the motor fibers of the facial nerve.

At the level of the cell nucleus, both positive and negative regulators of growth are necessary for normal control of cell proliferation. The positive regulators, protooncogenes, have products that function as growth factors, growth factor receptors, and signaling enzymes. Excessive production may occur that converts protooncogenes into oncogenes, resulting in significant neoplastic growth.

Negative regulators of cell growth are called tumor suppressor genes. Suppressor genes inhibit cellular proliferation at the level of the nucleus. The loss of tumor suppressor genes by mutation, deletion, or reduced expression aids in the conversion of normal cells to malignant phenotypes. The excessive stimulation of proto-oncogenes and the lack of inhibition of tumor suppressor genes ultimately lead to neoplastic proliferation. As the tumor grows, edema develops in surrounding tissues and intracranial pressure (ICP) increases. As the tumor continues to grow, it may interfere with the normal flow and drainage of CSF, causing an increase in ICP.

The brain compensates for increases by regulating the volume of the three substances in the following ways: limiting blood flow to the head, displacing CSF into the spinal canal, and increasing absorption or decreasing production of CSF.

Prolonged hemodynamic stress and local arterial degeneration at vessel bifurcations are believed to be a major contributing factor to the development and ultimate rupture of cerebral aneurysms. Bleeding spreads rapidly into the subarachnoid space and commonly into the intraventricular spaces and brain tissue, producing localized changes in the cerebral cortex and focal irritation of the cranial nerves and arteries. Increased ICP occurs, causing disruption of cerebral autoregulation and alterations in cerebral blood flow. Expanding intracranial hematomas may act as space-occupying lesions compressing or displacing brain tissue. Blockage of the ventricular system or decreased CSF absorption can result in hydrocephalus. Cerebral artery vasospasm occurs in the surrounding arteries and can further compromise cerebral blood flow, leading to cerebral ischemia and cerebral infarction.

An imbalance of the neurotransmitters is thought to be the underlying mechanism in depression. In a person with normal levels of neurotransmitters, serotonin and norepinephrine are released from one neuron and travel to another one, activating receptors. After the receptors are activated, the neurotransmitters are taken up by the presynaptic neuron. A patient with depression has inadequate levels of serotonin or norepinephrine, thus not allowing this smooth transmission of impulses.