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Signs of Central Nervous System Disorders

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Signs of Central Nervous System Disorders C H A P T E R 2 SIGNS OF CENTRAL NERVOUS SYSTEM DISORDERS Disorders of the brain and the spinal cord – the two major objects by touch (stereognosis). Neurologists often components of the central nervous system (CNS) – typi- describe loss of those modalities as “cortical” sensory loss. cally cause readily recognizable combinations of paresis, Pain sensation, a “primary” sense, is initially received sensory loss, visual deficits, and neuropsychologic disor- by the thalamus, from which it is relayed to the cortex, ders (Box 2.1). Such signs of CNS disorders differ from limbic system, and elsewhere. Because the thalamus is those of the peripheral nervous system (PNS) and both situated above the brainstem but below the cerebral differ from the signs of psychogenic disorders. Neurolo- cortex, most patients with cerebral lesions still perceive gists formulate their preliminary diagnosis and often ini- painful stimuli. For example, patients with cerebral tiate treatment on the basis of the patient’s history and infarctions may be unable to specify a painful area of their the examination, but if results of investigations – such as body, but they will still feel the pain’s intensity and dis- laboratory testing or magnetic resonance imaging (MRI) comfort (see Chapter 14). – contradict the initial clinical impression, they will Visual loss of the same half-field in each eye, homony- usually revise or at least reconsider it. mous hemianopia (Fig. 2.7), is a characteristic sign of a contralateral cerebral lesion. Other equally characteristic visual losses are associated with lesions involving the eye, SIGNS OF CEREBRAL HEMISPHERE LESIONS optic nerve, or optic tract (see Chapters 4 and 12). Because they are situated far from the visual pathway, Hemiparesis, usually accompanied by changes in reflexes lesions in the brainstem, cerebellum, or spinal cord do and muscle tone, is one of neurology’s most prominent not cause visual field loss. and reliable signs. Damage to the corticospinal tract, also Another conspicuous sign of a cerebral hemisphere called the pyramidal tract (Fig. 2.1), in the cerebrum or lesion is focal (partial) or focal-onset seizures (see Chapter brainstem above (rostral to) the decussation of the pyra- 10). In fact, the majority of focal seizures that alter aware- mids, causes contralateral hemiparesis (Box 2.2) with ness or induce psychomotor phenomena originate in the weakness of the arm and leg – and, if the lesion is high temporal lobe. enough, the lower face – opposite the side of the lesion. Damage to this tract within the spinal cord causes ipsilat- eral arm and leg or only leg paresis, but no face paresis. Signs of Damage of the Dominant, The division of the motor system into upper and lower Nondominant, or Both Cerebral Hemispheres motor neurons is a basic construct of clinical neurology. During the corticospinal tract’s entire path from the Although hemiparesis, hemisensory loss, homonymous cerebral cortex to the motor cranial nerve nuclei and hemianopia, and focal seizures may result from lesions of the anterior horn cells of the spinal cord, this tract either cerebral hemisphere, several neuropsychologic consists of upper motor neurons (UMNs) (Fig. 2.2). The deficits are referable to either the dominant or nondomi- anterior horn cells, which are part of the PNS, begin nant hemisphere. Neurologists usually ask a patient’s the lower motor neuron (LMN). Cerebral lesions that handedness when taking a history, but if this information damage the corticospinal tract cause signs of UMN injury is unavailable, because approximately 85% of people (Figs. 2.2–2.5): are right-handed, they assume with reasonable confi- • Paresis with muscle spasticity dence that the left hemisphere serves as the dominant • Hyperactive deep tendon reflexes (DTRs) hemisphere. • Babinski signs. Lesions of the dominant hemisphere may cause lan- In contrast, PNS lesions, including motor neuron dis- guage impairment, aphasia, a prominent and frequently eases (diseases of the anterior horn cells) and disorders of occurring neuropsychologic deficit (see Chapter 8). nerves (neuropathy), cause signs of LMN injury: Because the corticospinal tract sits adjacent to the lan- • Paresis with muscle flaccidity and atrophy guage centers, right hemiparesis often accompanies • Hypoactive DTRs aphasia (see Fig. 8.1). • No Babinski signs. Lesions of the nondominant parietal lobe tend to Another indication of a cerebral lesion is loss of certain produce one or more striking neuropsychologic distur- sensory modalities over one half of the body, i.e., hemi- bances (see Chapter 8). For example, patients may neglect sensory loss (Fig. 2.6). A patient with a cerebral lesion or ignore left-sided visual and tactile stimuli (hemi- characteristically loses contralateral position sensation, inattention). They may fail to use their left arm and leg two-point discrimination, and the ability to identify because they neglect their limbs rather than because of 7 8 SECTION 1 CLASSIC ANATOMIC NEUROLOGY BOX 2.1 Signs of Common CNS Lesions Cerebral hemisphere* Hemiparesis with hyperactive deep tendon reflexes, spas- ticity, and Babinski sign Internal Hemisensory loss capsule Homonymous hemianopia Focal (partial) seizures Aphasia, hemi-inattention, and dementia Pseudobulbar palsy Basal ganglia* Movement disorders: parkinsonism, athetosis, chorea, and Midbrain hemiballismus Postural instability Rigidity Brainstem Cranial nerve palsy with contralateral hemiparesis Pons Internuclear ophthalmoplegia (MLF# syndrome) Nystagmus Bulbar palsy Cerebellum Tremor on intention^ Impaired rapid alternating movements (dysdiadocho- kinesia)^ Medulla Ataxic gait Scanning speech Spinal cord Paraparesis or quadriparesis Spasticity Spinal cord Sensory loss up to a “level” Bladder, bowel, and sexual dysfunction FIGURE 2.1 ■ Each corticospinal tract originates in the cerebral *Signs contralateral to lesions cortex, passes through the internal capsule, and descends into #MLF, Medial longitudinal fasciculus the brainstem. The tracts cross in the pyramids, which are pro- ^Signs ipsilateral to lesions tuberances on the inferior portion of the medulla, to descend in the spinal cord mostly as the lateral corticospinal tract. The corticospinal tracts synapse with the anterior horn cells of the spinal cord, which give rise to peripheral nerves. Neurologists BOX 2.2 Signs of Common Cerebral Lesions often call the corticospinal tract the pyramidal tract because it crosses in the pyramids. The extrapyramidal system, which Either hemisphere* modulates the corticospinal tract, originates in the basal ganglia and cerebellum, and remains within the brain. Hemiparesis with hyperactive deep tendon reflexes and a Babinski sign Hemisensory loss Homonymous hemianopia damage produces several important disturbances that Focal seizure Dominant hemisphere psychiatrists are likely to encounter in their patients. One Aphasia: fluent, nonfluent, conduction, or isolation of them, pseudobulbar palsy, best known for producing Gerstmann syndrome: acalculia, agraphia, finger agnosia, emotional lability, results from bilateral corticobulbar tract and left–right confusion damage (see Chapter 4). The corticobulbar tract, like its Alexia without agraphia counterpart the corticospinal tract, originates in the Nondominant hemisphere motor cortex of the posterior portion of the frontal lobe. Hemi-inattention It innervates the brainstem motor nuclei, which in turn Anosognosia innervate the head and neck muscles. Traumatic brain Constructional apraxia injury (TBI), multiple cerebral infarctions (strokes), and Both hemispheres frontotemporal dementia (see Chapter 7), are apt to Dementia Pseudobulbar palsy strike the corticobulbar tract, as well as the surrounding frontal lobes, and thereby cause pseudobulbar palsy. *Signs contralateral to lesions Damage to both cerebral hemispheres – from large or multiple discrete lesions, degenerative diseases, or meta- bolic abnormalities – also causes dementia (see Chapter paresis. When they have left hemiparesis, patients may 7). In addition, because CNS damage that causes demen- not appreciate it (anosognosia). Many patients lose their tia must be extensive and severe, it usually also produces ability to arrange matchsticks into certain patterns or at least subtle physical neurologic findings, such as hyper- copy simple forms (constructional apraxia, Fig. 2.8). active DTRs, Babinski signs, mild gait impairment, and As opposed to signs resulting from unilateral cerebral frontal lobe release reflexes. However, many neurode- hemisphere damage, bilateral cerebral hemisphere generative illnesses that cause dementia, particularly 2 SIGNS OF CENTRAL NERVOUS SYSTEM DISORDERS 9 A UMN Brain Normal UMN lesions Spinal cord B Afferent limb C LMN LMN LMN efferent Peripheral nerve lesion limb Quadriceps muscle tendon ∅ ∅ A B C FIGURE 2.2 ■ A, Normally, when neurologists strike a patient’s quadriceps tendon with a percussion hammer, the maneuver elicits a DTR. In addition, when they stroke the sole of the foot to elicit a plantar reflex, the big toe bends downward (flexes). B, When brain or spinal cord lesions injure the corticospinal tract, producing upper motor neuron (UMN) damage, DTRs react briskly and forcefully, i.e., DTRs are hyperactive. As another sign of UMN damage, the plantar reflex is extensor (a Babinski sign). C, In contrast, peripheral nerve injury causes lower motor neuron (LMN) damage, the DTR is hypoactive and the plantar reflex is absent. FIGURE 2.3 ■ This patient shows right hemiparesis with weak-
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