An Approach to Neurologic Symptoms

Steven L. Lewis

key points

A careful neurologic history is the cornerstone of neurologic diagnosis.
The goal of the neurologic history, followed by the examination and appropriate diagnostic studies, is to determine, first, where in the nervous system the dysfunction lies and, next, how that dysfunction occurred.
Using neurologic terminology to describe the likely site of neurologic dysfunction can be very helpful in categorizing patients’ symptoms and signs.
Even a very basic and simplified understanding of neuroanatomy can be of great benefit in neurologic diagnosis.
Recognizing the temporal course of a patient’s neurologic illness is critical in determining the likely disease mechanism.

In neurologic diagnosis, individual symptoms and constellations of symptoms can be of telling diagnostic importance both anatomically and etiologically. Thus, a detailed neurologic history that puts together various symptoms and their temporal development can help to define neurologic entities with significant precision; the role of the subsequent neurologic examination is to look for evidence to support, or refute, the diagnostic hypothesis that was generated by analysis of the careful neurologic history.

COMMON NEUROLOGIC TERMS

Before proceeding with a discussion of specific neurologic symptoms, it is worthwhile to define some terms that can be useful in characterizing neurologic symptom complexes. These words are used to indicate certain localizations of pathology (Table 2.1).

Encephalopathy means disease of the brain. Although theoretically the term encephalopathy could refer to any process involving any
part of the brain, it generally is used to mean dysfunction that involves the entirety of both cerebral hemispheres. Thus, the terms encephalopathy and diffuse encephalopathy are synonymous. An example of a common type of encephalopathy is a metabolic encephalopathy, such as that caused by hepatic, uremic, or other metabolic dysfunction.

TABLE 2.1 Common Terms Used to Describe Localizations of Neurologic Dysfunction

Term	Meaning
Encephalopathy	Disease of brain (usually refers to diffuse brain dysfunction)
Myelopathy	Disease of spinal cord
Radiculopathy	Disease of nerve root
Neuropathy	Disease of nerve
Myopathy	Disease of muscle

Myelopathy means disease of the spinal cord. A patient with any symptoms or signs that are caused by spinal cord dysfunction has a myelopathy. An example of a common type of myelopathy is a compressive myelopathy caused by a tumor or other mass lesion compressing the spinal cord, causing weakness, sensory loss, and spasticity below the level of the compression.

Radiculopathy, disease of the nerve roots (radix is Latin for root; a radish is a root vegetable), is the term used for any process involving single or multiple nerve roots in the cervical, thoracic, or lumbar spine. For example, a herniated lumbar disc between the fourth and fifth lumbar spine might cause an L5 radiculopathy; Guillain-Barré syndrome would cause a polyradiculopathy as a result of dysfunction of multiple nerve roots.

Neuropathy means disease of a nerve. The term means dysfunction of one (mononeuropathy), several (mononeuropathy multiplex), or many/diffuse (polyneuropathy) peripheral nerves. Dysfunction of a cranial nerve would be called a cranial neuropathy. Myopathy refers to any disease of muscle.

These generic terms are very helpful to the clinician in categorizing sites of pathology or dysfunction. A specific causative lesion, or causative process, is not conveyed by any of these terms. Unless there is a preceding adjective (e.g., compressive myelopathy or demyelinative polyneuropathy), a cause or mechanism is not implied. Likewise, substitution of the suffix -itis for -pathy (e.g., myositis instead of myopathy) implies, specifically, an inflammatory process, rather than an as-yet-unknown process affecting that region of the nervous system.

AN APPROACH TO SPECIFIC NEUROLOGIC SYMPTOM COMPLEXES

The essential elements of the neurologic diagnostic process are an accurate and detailed history, followed by a neurologic examination. Imaging and laboratory studies follow, as appropriate.

▪ SPECIAL CLINICAL POINT: The goals of neurologic diagnosis are to determine, first, where in the nervous system the problem lies, and, next, to determine how the dysfunction occurred.

This section discusses the “where” part of the neurologic formulation using the history and examination to evaluate several specific symptom complexes (mental status changes, weakness, sensory symptoms, and gait disorders). Using the temporal course of the evolution of symptoms to help determine the mechanism of dysfunction (the “what” part) will be discussed later in this chapter.

MENTAL STATUS CHANGES

When confronted with a patient who has had a mental status change, the clinician should try to determine whether there is an alteration in the level of consciousness or an alteration of the content of consciousness. Alterations in the level of consciousness manifest in the continuum
between drowsiness and coma. They result either from dysfunction of both cerebral hemispheres, dysfunction of the upper brainstem, or a combination of hemispheric and upper brainstem dysfunction. The clinical approach to the patient who presents with an alteration in level of consciousness is discussed in more detail in Chapter 5.

▪ SPECIAL CLINICAL POINT: A major goal of the neurologic examination of patients with an alteration of the level of consciousness is determining whether there is evidence for focal brainstem dysfunction.

If brainstem function is intact, the cause of the problem is unlikely to be the result of a focal structural brainstem process; it is more likely the result of a diffuse encephalopathic process. The actual processes that may affect the level of consciousness are vast and are discussed in more detail in Chapter 5.

Neurologic processes can affect the mental status of patients, however, by affecting the content of consciousness without necessarily altering the level of consciousness. Alterations in the content of consciousness are exemplified by psychiatric disorders or by neurologic disorders that affect memory, language, awareness, or global intellectual functioning. Patients with chronic dementing illnesses (Chapter 16) usually have normal alertness despite the deterioration in cognitive functioning. Patients with aphasia—particularly those with fluent aphasias—often appear to be confused. More careful attention to the patient’s speech pattern to determine the presence of paraphasic errors and neologisms (“new words” without meaning) often will help the clinician determine that the “confused” patient is actually aphasic; the presence of aphasia is usually a clue to focal dysfunction in the dominant (usually left) hemisphere. Patients with lesions affecting the right hemisphere also may appear to be “confused,” neglectful, and unaware, whereas they actually have neglect of the left side of space and may be oblivious of their deficit (anosagnosia) because of the nondominant hemisphere dysfunction.

WEAKNESS

“Weakness” as a patient complaint may have several possible meanings, besides the usually presumed meaning of a decrease in motor function in one or several extremities. The clinician should keep in mind that some patients might use the term “weakness” to describe generalized fatigue, malaise, or asthenia. Some patients might even describe a symptom such as the generalized bradykinesia of parkinsonism (Chapter 10) as weakness. As in all neurologic diagnosis, an accurate history and examination should help clarify what symptoms the patient is actually describing. Muscular fatigue, although very nonspecific, suggests the possibility of a disorder of the neuromuscular junction, such as myasthenia gravis (see Chapter 19), or a disease of muscle (myopathy), in addition to the many primarily nonneurologic processes that can cause generalized malaise and fatigue.

The following are definitions of some common terms used to describe decreases in motor function. Paresis refers to muscular weakness but not complete paralysis. Plegia is the term used to describe complete paralysis. Monoparesis and monoplegia are terms sometimes used to describe weakness or paralysis in one extremity. Hemiparesis and hemiplegia refer to weakness or paralysis in the arm and leg on one side of the body. Paraparesis and paraplegia describe weakness or paralysis in both legs, and quadriparesis and quadriplegia (sometimes alternatively called tetraplegia) denote weakness or paralysis in all four extremities.

Muscular weakness can occur as a result of dysfunction at any level of the central or peripheral nervous system. To illustrate this, it is worth considering the neuroanatomic pathway for muscle movement. The pathway for muscle movement begins in nerve cells that are located on the precentral gyrus of each frontal lobe (the upper motor neurons). The axons from these
nerve cells comprise the corticospinal tract. The corticospinal tracts travel through the white matter of each cerebral hemisphere, through the internal capsule, and further downward into the brainstem, where each corticospinal tract crosses in the low medulla to the opposite side. From the medulla, the corticospinal tracts travel downward through each side of the spinal cord.

Within the spinal cord, the corticospinal tract on each side synapses with nerve cells in the anterior horns located in the spinal cord gray matter (the lower motor neurons). Axons from these second-order neurons become the cervical, thoracic, and lumbosacral nerve roots. The cervical nerve roots then form the brachial plexus, and the nerves that are formed in the brachial plexus travel into the upper extremities and innervate the muscles of the upper extremities. The lumbar nerve roots travel downward within the lumbar spinal canal as the cauda equina, before exiting and forming the lumbosacral plexus and ultimately forming the nerves that innervate the lowerextremity musculature.

▪ SPECIAL CLINICAL POINT: A lesion at any level of the upper and lower motor neuron pathway, from the cerebral cortex to the muscles themselves, can cause weakness.

The location of this lesion causing weakness, or a history of weakness, is not always immediately obvious, even to an experienced clinician who has performed an accurate history and examination. However, there are typical, or classic, patterns of muscle weakness that lesions at various levels of the pathway for motor function usually will produce. Recognition of these typical patterns can be very helpful in attempting to decide on possible localizations of pathology in patients who present with motor weakness.

Upper Motor Neuron Lesions

Lesions that cause dysfunction of the corticospinal tracts are called upper motor neuron lesions; their distinctive features, in addition to weakness, include increased or pathologic reflexes, and increased tone and spasticity in chronic lesions. It also should be recognized that these classic findings of upper motor neuron dysfunction might not always be evident. Upper motor neuron syndromes can result from lesions of the corticospinal tract at various levels of the central nervous system. Further clinical details help to specify whether the lesion is cortical, subcortical, or in the spinal cord. When symptoms of transient motor dysfunction occur that have resolved by the time of the examination, however, no abnormalities would be expected on examination, and the site of the lesion must be inferred by the patient’s description of the areas of transient weakness and associated symptoms.

Hemispheric motor cortex lesions involving the cortical motor neurons of the lateral surface of one hemisphere usually cause upper motor neuron weakness of the contralateral face and arm, with less weakness of the leg. A lesion in this region, like all corticospinal tract lesions, often will cause predominant weakness in the extensors of the arm and flexors of the leg, with relative preservation of strength in arm flexors and leg extensors. As such, the affected arm is held mildly flexed while walking and the leg is overextended, causing it to drag stiffly, sometimes catching the toe. Hemispheric motor cortex lesions involving the medial aspect of one frontal lobe will predominantly cause contralateral leg weakness. Weakness resulting from cortical lesions often is also accompanied by other signs of cortical dysfunction, giving a clue to the localization of the problem. For example, left hemisphere cortical lesions often are accompanied by abnormalities of language function. Right hemisphere cortical lesions often are accompanied by denial of the left-sided weakness (anosagnosia) or even unawareness of the presence of the left extremities (asomatagnosia). Any complex behavioral change of these types suggests that the upper motor neuron lesion is cortical. Cortical lesions causing weakness are often also
accompanied by some contralateral sensory disturbance because of the proximity of the cortical sensory neurons to the motor cortex.

Deep hemispheric or internal capsule lesions also will cause weakness of the contralateral body, but without accompanying signs of cortical dysfunction. Lesions affecting the corticospinal tract fibers in the posterior limb of the internal capsule may produce a characteristic pure motor hemiparesis (or hemiplegia) involving the contralateral face, arm, and leg. This is characterized by significant weakness of one side of the body without sensory disturbance or signs of cortical dysfunction such as aphasia. This distinctive form of isolated weakness occurs because the corticospinal fibers from a large area of the motor cortex all lie close together in the internal capsule, segregated from the sensory fibers, and deep to the cortical structures. In contrast, a hemispheric lesion that would be large enough to cause significant weakness of an entire side of the body most likely also would involve sensory signs or symptoms and signs of cortical dysfunction.

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