Lemniscus

lateral ventricle ventricle lateral ventricle

Figure 9-23

4) Hemiballismus—a sudden wild flail-like movement of one arm.

Cerebral Cortex

Lesions to the nervous system may lead to simple or complex levels of dysfunction depending upon the area involved. For instance, if one asks a patient to put on a polo shirt and his left brachial plexus is severed, he will only use his right arm, as his left arm is paralyzed. The cerebellum and basal ganglia represent a step further in levels of functioning. With a cerebellar lesion, the patient may perform the act awkwardly, e.g. overshooting the mark, or with tremor. With basal ganglia lesions there may be unexpected, unplanned totally irrelevant movements, beyond the realm of awkwardness, e.g. a sudden flail-like movement, etc. In the cerebral cortex, unless the lesion is in the primary motor area wherein paralysis may result, a higher level of dysfunction may be found, e.g. the patient trying to get his head into the sleeve or trying other inadequate orientations.

In speech, a lesion of CN10 may result in hoarseness (laryngeal dysfunction). When cranial nerves 10, 1'2 or 7 are involved, there may be difficulty with the "KLM" sounds; i.e. the sounds "Kuh, Kuh, Kuh" test the soft palate (CN10), "LA, LA, LA," the tongue (CN12) and "MI, MI, MI" the lips (CN7). With lesions in the speech areas of the cerebral cortex, the deficit may involve higher levels of speech organization—the deletion of words or inclusion of excessive or inappropriate words. In psychiatric disturbances, the level of dysfunction is even higher with abnormalitites in the entire pattern of thought organization.

It is similar for the sensory pathways. Simple anesthesia (total sensory loss) may result from lesions between the primary sensory cortex and the body periphery. In other brain areas, the patient may have difficulty in comprehending the incoming information. For instance, a lesion to the optic tract results in homonymous hemianopia (neither eye can see the environment contralateral to the lesion). In lesions to cortical areas 18 and 19 the patient sees but may not recognize what he is looking at.

Complex cerebral receptive disabilities are called agnosias. Complex cerebral motor disabilities are aprax-ias. Often the two are difficult to distinguish.

When language function is involved, the disabilities are termed aphasias. Aphasia may be receptive (i.e. reading, listening) or motor (i.e. writing, talking). For aphasia to occur, the lesion must be in the dominant hemisphere, which is the left hemisphere in right handed people and in many (but not all) left handed people.

Fig. 9-24. Major regions of the cerebrum. The shaded area indicates the region of the cerebral cortex involved with aphasia. Subdivisions of this area are logical. Lesions in the anterior part of this area, near the motor cortex, tend to result in expressive aphasia. Lesions more posterior, near the auditory and visual cortex, result in receptive aphasia. Lesions nearer the visual cortex result in inability to read (alexia). Lesions near the auditory cortex result in inability to understand speech. Actually, difficulty in talking may result from both anterior or posterior lesions. Following lesions in the more anterior regions of the aphasic zone, speech distur-

bances tend to be nonfluent; the patient omits nouns and connector words like but, or and and. In the more posterior regions his words are plentiful or even excessive, but he crams into his speech inappropriate word substitutes, circumlocutions and neologisms—a word salad. Presumably, this is because the ability to speak also depends on the ability to understand what one is saying. Thus, if the aphasic area near the auditory cortex is involved, this will also result in a defect in speech.

Lesions to corresponding areas of the non-dominant hemisphere do not result in aphasia, but rather in visual or auditory inattention to the left environment or to general unawareness of the concept of "left." The patient may deny he has any neurological deficit despite a dense hemiplegia and left visual field defect.

Specific cerebral cortical regions and the effects of lesions are listed below.

Area 4 (the primary motor area). Lesions result in initial flaccid paralysis followed in several months by partial recovery of function and a possible Babinski reflex; spasticity and increased deep tendon reflexes may occur if area 6 (the supplemental motor area) is included.

Lesions to area 8 (the frontal eye fields) result in difficulty in voluntarily moving the eyes to the opposite side.

Areas of the frontal cortex rostral to the motor area are involved in complex behavioral activités. Lesions result in changes in judgement, abstract thinking, tact-fulness and foresight. Symptoms may include irresponsibility in dealing with daily affairs, vulgar speech and clownish behavior.

Areas 44,45 (Broca's speech area). The patient with a lesion in this area experiences motor aphasia, but only when the dominant hemisphere is involved. The patient knows what he wants to say but speech is slow, deleting many prepositions and nouns.

Areas 3,1,2 (primary somesthetic area). Lesions produce contralateral impairment of touch, pressure and proprioception. Pain sensation will be impaired if the lesion lies in the secondary somesthetic sensory area (Fig. 9-24) which receives pain information.

Areas 41,42 (auditory area). Unilateral lesions have little effect on hearing owing to the bilateral representation of the auditory pathways. Significant auditory defects generally involve either CN8 or its entry point in the brain stem, for bilateral representation begins beyond this point in the brain stem.

Area 22 (Wernicke's area). Lesions in the dominant hemisphere result in auditory aphasia. The patient hears but does not understand. He speaks but makes mistakes unknowingly owing to his inability to understand his own words.

Area 40 (supramarginal gyrus). Lesions in the dominant hemisphere result in tactile and proprioceptive agnosia, and a variety of other problems, such as confusion in left-right discrimination, disturbances of body-image, and apraxia, by cutting off impulses to and from association tracts that interconnect this area with nearby regions.

Area 39 (angular gyrus). Lesions in the dominant hemisphere may result in alexia and agraphia (inability to read and write).

Areas 17,18, 19. Total destruction causes blindness in the contralateral visual field. Lesions to areas 18 and 19 alone do not cause blindness but rather difficulty in recognizing and identifying objects (visual agnosia).

The silent area is believed to function in memory storage of visual and auditory information and is implicated in hallucinations and dreams. Epileptic attacks originating in this region may be associated with amnesia, auditory hallucinations, and the deja vu phenomenon.

Localization of Neurologic Problems

In approaching a patient with a neurologic problem, there are a number of key questions that help establish the localization of the lesion:

1) Is there a dermatome deficit (Fig. 9-25)? If so, this suggests a peripheral nerve lesion, as the central nervous system is not organized according to dermatomes. Lesions to central nervous system sensory pathways more likely will cause a general loss of sensation in an extremity than the strip-like deficit of a dermatome lesion.

Fig. 9-25. Dermatomes, the distribution of sensory nerves on the skin.

2) Is there localized pain? Lesions to sensory areas of the central nervous system tend to cause loss of pain rather than pain itself. The presence of localized pain suggests irritation of a peripheral nerve or nerve root.

3) Are there upper or lower motor neuron signs (Fig. 9-12)? This will help pinpoint whether the lesion lies at the CNS (UMN) or peripheral nerve (LMN) level.

4) Is there a dissociation of sensory loss, i.e. loss of pain-temperature in one extremity, but loss of proprioception in the other extremity? This suggests a spinal cord lesion, because the sensory pathways cross at different levels of the spinal cord, but have all crossed (ex cept for the spinocerebellar tract) by the time they reach the brain stem.

5) Is there cranial nerve involvement? If so, this establishes the localization of the lesion above the foramen magnum, where the spinal cord becomes the brainstem.

6) Is there some combination of a cranial nerve deficit on one side of the face, and an extremity deficit on the other side (for example, a dilated fixed pupil on the right, combined with paralysis or sensory loss of the left upper and lower extremities)? If so, this indicates a brainstem lesion, because lesions below the brainstem would not cause cranial nerve deficits, and lesions above the brain stem would cause deficits restricted to the contralateral environment.

7) Which cranial nerves are involved? If there is a unilateral loss of CN3 (pupil enlarged, unresponsive to light; failure of the eye to adduct), or unilateral loss of CN6 (failure of the eye to abduct), or facial (CN7) weakness on one entire side of the face (i.e. manifest in both the upper and lower face), or atrophy and fasciculations of one side of the tongue, this suggests either a brainstem injury or injury to the nerve more peripherally. Cerebral lesions would not cause such deficits, due to the bilateral innervation of these cranial nerves.

Bilateral lesions of the cerebral cortex or internal capsule (the area where cerebral cortex fibers funnel into the brainstem) may result in pseudobulbar palsy, in which there are multiple cranial nerve deficits. The patient then experiences difficulties with facial expression, movement of the tongue, chewing, swallowing, speech and breathing. There also may be inappropriate spells of laughing or crying as part of the syndrome.

8) Is there awkwardness of movement? Weakness in an extremity can cause awkwardness of movement, but in the absence of weakness, one must ask whether the problem lies at the cerebellar level or the basal ganglia? Awkwardness of intended movements (ataxia) or tremor on intended movements suggest a lesion of the cerebellum or its connecting pathways. Involuntary movements (e.g. resting tremor, chorea (uncontrolled awkward jerky movements), athetosis (writhing movements), hemiballismus (wild flinging movements of an extremity) are characteristic of basal ganglia lesions.

9) It may be difficult to differentiate a lesion in the cerebral cortex from one in the internal capsule (the region in the core of the brain where motor and sensory fibers funnel into and out of the brain stem). The presence of a higher level dysfunction suggests a cerebral cortex lesion. This may include an agnosia (complex receptive disability, e.g. loss of ability to understand what one is reading while retaining the ability to see), apraxia (complex motor disability, such as putting on one's pants backwards), and aphasia (complex speech disturbance, as opposed to simple hoarseness or monotone).

Figure 9-25

The Electroencephalogram (EEG)

The EEG is a record of the summed underlying neuronal activity of the brain, as sampled in a number of areas over the scalp.

Fig. 9-26. Normal EEG patterns. Brain waves vary in their frequency. They tend to be fastest when the subject is most alert (beta waves, > 13 waves/sec (also called Hertz/second or just Hz). Alpha waves are somewhat slower (8-13Hz/sec) and occur in a state of quiet awareness, but also in the dream phase (REM, or rapid eye movement phase) of sleep. Theta waves (4-7Hz) are slower and occur in drowsiness, whereas Delta waves (<4Hz) are even slower, occurring in deep sleep or in the pathologically depressed brain. A flat EEG occurs in brain death, but can also occur in certain states of drug overdosage.

Fig. 9-27. EEG patterns in epilepsy. Analysis of the EEG can be useful diagnostically. Diffuse slowing of the waves is often found in organic mental syndrome. Focal localization of the slowing often points to a discrete neurologic lesion, although MRI scans and other imaging procedures are generally much more useful in localizing a lesion. In epilepsy, abnormal discharges are seen on

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Figure 9-27

the EEG, which contains abnormal sharp waves or spikes. In grand mal epilepsy, there is diffuse rapid, high amplitude firing that coincides with a diffuse epileptic seizure. The patient may have shaking of the extremities, tongue biting, and urinary and fecal incontinence secondary to diffuse electrical seizure discharges. In focal ("Jacksonian") seizures, which involve seizures of a limited area of the body, e.g. the arm, the seizure activity is more localized, and often can be traced to a focal scar or tumor as the factor that generates the seizure. In petit mal epilepsy, a condition that mainly affects children, there are brief unresponsive periods of staring, along with a "spike and dome" pattern to the EEG. In psychomotor seizures, there may be organized patterns of uncontrollable abnormal social behavior, rather than shaking movements. Uncinate seizures, which originate in the uncus of the temporal lobe, are characterized by the experience of abnormal smells, such as burning rubber.

THE SPECIAL SENSES: VISION

Fig. 9-28. Sagittal section through the human eye.

It is difficult to play billiards using eyeballs, as the eye is not perfectly spherical. The cornea is too steeply curved. This steep curvature enables the cornea to perform most of the refraction (bending and focusing) of light entering the eye. The cornea provides a coarse, nonvariable focus. The lens also focuses light, but only performs the fine variable adjustments. Contact lenses artificially alter the curvature of the front of the eye, thereby changing the focus.

The eye has three chambers: the anterior chamber (A.C.) (in front of the iris), the posterior chamber (P) (between the iris and the lens), and the vitreous chamber (behind the lens). The anterior and posterior chambers contain the clear, watery aqueous humor produced constantly by the ciliary body. Aqueous humor (arrows) exits the eye via the circular canal of Schlemm (S), which lies in the angle between the cornea and iris. The canal of Schlemm communicates directly with venous circulation. Blockage of aqueous out-

Figure 9-28

flow results in increased intraocular pressure, termed glaucoma.

The ciliary body not only produces aqueous humor, but also contains a ring of ciliary muscle (Fig. 9-29) that is attached to the lens via fine, ligamentous zonule fibers. Contraction of the ciliary muscles affects the shape of the lens, thereby changing its focus—the process of accommodation.

Fig. 9-29. Posterior view of the ciliary muscle ring.

The mechanism of accommodation is more easily understood by first considering the mechanism of pupillary expansion (dilation) and constriction, as follows. The iris contains circular (constrictor) muscles at the pupillary border, and radial (dilator) muscle fibers (Fig. 9-30).

Fig. 9-30. Constrictor and dilator muscles of the iris. Note how contraction of the radial fibers would dilate the pupil. Contraction of the constrictor muscles decreases the circumference of the ring; therefore, the pupil constricts. The ciliary muscles, although more complex than the iris constrictor muscles, in a sense act similarly. Contraction of muscles in the ciliary ring narrows the diameter of the ring. This decreases the tension of the zonules, and releases tension on the lens. The lens then springs back into a thicker, rounder shape leading to a stronger focus (accommodation). Thus, accommodation is the process in which the ciliary muscles contract, thereby relaxing tension on the lens and enabling one to focus closer on an object.

Figure 9-29

Opacities in the lens (cataracts) may obstruct vision, particularly when they are positioned centrally, in the posterior aspect of the lens ("x" in Fig. 9-28). For optical reasons, cataracts in the anterior aspect of the lens or at the lens periphery tend to cause less visual loss.

The vitreous chamber contains vitreous humor, a thick gel. Unlike the aqueous humor, vitreous humor is no longer produced in the mature eye. Vitreous that is lost inadvertently from the eye during intraocular surgery cannot be replaced; fortunately, normal saline or aqueous humor may be substituted.

The eye has three main coats—the retina, choroid (a very vascular, pigmented structure), and sclera (the

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