Brain Stem Dysfunction In Disease

Most people are used to the idea that dysfunction of one cerebral hemisphere can lead to paralysis of the other side of the body. This may occur, for example, with ischemia of brain tissue supplied by the internal carotid artery or the middle cerebral artery. Sudden impairment of the blood supply is also a common cause of brain stem dysfunction, but in this case it is the vertebrobasilar system of arteries that is at fault. Other disease processes (infection, neoplasm, and inflammation) may also affect brain stem function. The neurological symptoms and signs of brain stem dysfunction depend on the precise subregion affected.

Dysfunction of the upper brain stem (especially the more dorsal portions of the rostral pons), the midbrain region just ventral to the aqueduct, and the thalamus can cause the patient to be drowsy, stuporose, or unconscious. This presumably reflects damage to the ascending pathways described in Section IV.A.

Impairment of brain stem eye movement control systems includes supranuclear palsies (upper moto-neuron lesions), internuclear ophthalmoplegias, and strabysmus or squint (crooked eyes) reflecting dysfunction of the relevant lower motoneurons or of the oculomotor, trochlear, and abducens nerves (cranial nerves III, IV, and VI) or dysfunction of the muscles moving the eyeballs.

In a supranuclear palsy, as occurs in a neurodegen-erative disease known as Steele-Richardson syndrome or progressive supranuclear palsy, both eyes move conjugately (together) but particular directions of movement (particularly looking up) are poorly executed. Internuclear ophthalmoplegia reflects damage to the medial longitudinal fasciculus, a bundle of axons coordinating the relevant pontine and midbrain mo-toneurons, as may occur with small demyelinating lesions in the disease known as multiple sclerosis. When the patient tries to look to the right, the left eyeball fails to turn inward (adduct) and the out-turned right eyeball develops nystagmus.

Young children with a chronic strabysmus must be treated or the brain will suppress the image from one eye (a condition known as amblyopia) so that the individual never develops stereoscopic (binocular) vision. Acute lower motoneuron lesions usually cause double vision (diplopia), which is worse when the patient attempts to look in the direction controlled by the affected nerve. This symptom occurs partially because there is minimal feedback to the brain concerning the actual spatial position of the eyeball (contrast, for example, the accuracy with which we can judge the spatial position of the tip of the tongue). The brain sends the appropriate movement commands to the cranial motoneurons controlling the eyeball muscles and then interprets visual inputs as if the commands have been successfully executed. If one eyeball is misaligned, the brain makes a mistake and the result is double vision, not a sensation that the eyeball is in the wrong position.

A person may suddenly lose the ability to move one side of the face so that it may be impossible to close one eye or to wrinkle up the forehead on one side. The corner of the mouth may droop on one side. This condition may occur with damage to cranial nerve VII (facial) in its course within the pons or, more commonly in the condition known as Bell's palsy, when a peripheral segment of nerve VII is inflamed by a viral infection.

Dysfunction of the vestibular apparatus or its connecting brain stem pathways can induce the sensation of vertigo, sometimes associated with nausea and vomiting. Vertigo, tinnitus, and deafness also occur in Mennier's disease or with an acoustic neuroma, a tumor of the intracranial portion of the vestibulocochlear nerve (cranial nerve VIII). Brain stem dysfunction can also cause difficulty with speaking or swallowing.

The pathways connecting forebrain regions with the spinal cord can also be affected during their course through the brain stem. The major motor pathways from each side of the forebrain travel down the front of the midbrain, pons, and medulla, close to the midline, so that basilar artery ischemia may affect both these "pyramidal tracts,'' resulting in motor paralysis on both sides of the body. In severe brain stem dysfunction, the patient may be unable to move any one of the four limbs (quadraplegia) or even the head or any of the facial muscles so that the only way the patient can signal "yes'' or "no'' is by moving the eyes from side to side. Such patients, with normal consciousness and normal higher intellectual function, are described as being "locked in.''

Locked in patients are quite different from patients in the so-called "chronic vegetative state.'' This condition follows damage to the dorsal portion of the upper part of the brain stem with preservation of function in the pons and medulla. Patients in the chronic vegetative state have no voluntary movement and, presumably, no consciousness or thought processes. However, they have reflex movements and they can still breath and swallow. Their cardiovascular, renal, and gastrointestinal function is stable. If such patients are fed with nutritious food and their bowel and bladder wastes are dealt with, they may survive for years. In such patients, the preservation in the limbs of complex motor responses, such as movement of the arms during yawning, may give false hopes to relatives watching at the bedside.

Some patients do recover from a vegetative-like state so it may be difficult to decide whether or not to render life support to a particular patient for an extended time. A useful guide can be obtained from a knowledge of the cause of the brain stem injury, aided by modern investigative techniques such as magnetic resonance imaging (MRI). If a person becomes unconscious from a viral infection in the upper brain stem and the MRI is normal, then there is a chance of

Squiggly Line Brain Stem Mri

Figure 6 Magnetic resonance images in sagittal, coronal, and transverse planes through the brain stem of a 62-year-old woman with an ischemic stroke in the medial pons (arrows). The infarcted area of the brain is indicated by the dotted lines (MRI courtesy of the Department of Diagnostic Imaging, Flinders Medical Centre, Adelaide).

Figure 6 Magnetic resonance images in sagittal, coronal, and transverse planes through the brain stem of a 62-year-old woman with an ischemic stroke in the medial pons (arrows). The infarcted area of the brain is indicated by the dotted lines (MRI courtesy of the Department of Diagnostic Imaging, Flinders Medical Centre, Adelaide).

recovery to a normal life even if the person remains unconscious for months. If a motor vehicle accident or an ischemic stroke is the cause of the upper brain stem dysfunction, and the MRI shows strong evidence of structural damage, then recovery after being unconscious for as long as 1 month or even 1 week is extremely unlikely.

Extensive damage to the lower brain stem by any disease process usually ends the person's life because neural circuitry mediating vital respiratory and/or cardiovascular control no longer functions.

Sometimes, a small area of the brain stem can be affected by a focal disease process. The precise location of the damage can often be specified by particular combinations of physical signs, as in the following case: A 62-year-old woman presented with onset of motor dysfunction of her right hand and right leg (right hemiparesis), occurring in a stuttering fashion over a few hours. She was presumed to have ischemic damage (a cerebral infarct, a type of stroke) to the motor pathways in the left cerebral hemisphere (in the forebrain). However, the next day she developed double vision and was found to be unable to move her left eye to the left (failure of abduction to the left), indicating damage to the intramedullary course of the left sixth cranial nerve (abducent nerve). The combination of right hemiparesis and left sixth nerve palsy implied that the ischemic damage had occurred in the left lower brain stem, anteriorly where the intrapontine fibers of the left sixth nerve pass close to the descending corticospinal motor pathway, above the level where it crosses to the contralateral side (at the lower border of the medulla oblongata). An MRI scan confirmed the presence of a lesion situated anteriorly and medially on the left side of the pons (Fig. 6).

See Also the Following Articles

CEREBELLUM • CRANIAL NERVES • HINDBRAIN • HOMEOSTATIC MECHANISMS • NEUROANATOMY •

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