Neurology Physical Examination
Margaretha Palone
Solid knowledge of the basic principles of the various disease processes is essential for obtaining a good history. As Goethe stated, "The eyes see what the mind knows." To this end, the reader is referred to the literature about the natural history of diseases. The purpose of this article is to highlight the process of the examination rather than to provide details about the clinical and pathologic features of specific diseases.
The neurologic examination is one of the most unique exercises in all of clinical medicine. Whereas the history is the most important element in defining the clinical problem, neurologic examination is performed to localize a lesion in the central nervous system (CNS) or peripheral nervous system (PNS). The statement has been made, "History tells you what it is, and the examination tells you where it is." The history and examination allow the neurologist to arrive at the etiology and pathology of the condition, which are essential for treatment planning. [4, 5]
Unlike many other fields of medicine in which diseases are visible (eg, dermatology, ophthalmology) or palpable (eg, surgery), neurology is characterized by conditions that may be detected only by applying specific examination techniques and logical deduction, except when telltale cutaneous markers or other stigmata suggest the diagnosis. Considerable insight and intuition are required to interpret the symptoms and signs observed during neurologic examination. These features make the neurologic history and physical examination both challenging and rewarding. Neurologic examination can be particularly helpful for critically ill patients because many patients admitted to the intensive care unit (ICU) have pre-existing or acquired neurological disorders which significantly affect their short-term and long-term outcomes. [6]
A properly performed neurologic examination may take 90 minutes or even longer for the novice. Experienced neurologists take substantially less time and can frequently grasp the essential features of a clinical condition quickly. What might appear to be a complex problem of localization for the referring physician may turn out to have a simple explanation, and the neurologic consultation may help to avoid extensive testing.
With the advent of CT scanning in the early 1970s, the future clinical role of the neurologist was questioned. During one of his visits to the United States, Dr. McDonald Critchley was asked what he thought would be the future of neurology in the era of CT. His answer was most enlightening: "CT scanning will take away the shadows of neurology, but the music will still remain." These prophetic words still ring true despite the advent of MRI, positron emission tomography (PET), and functional neuroimaging of all types.
It has been said that "neurology owes more to its disorders than those disorders owe to neurology." This is because much knowledge has come from previous observations of neurologic conditions, because the eponyms for the diagnoses were sometimes long, and because so little was previously offered in the terms of cures such that the specialty was ridiculed as one that was "long on diagnosis and short on treatment." Fortunately, technologic advances have changed that perception.
In examining a patient, abnormalities of function lead to localization and, eventually, to the pathophysiology. [7] For the purpose of simplicity, the neurologic examination is divided into several steps. When mastered, these steps become second nature to the examiner, and the process of evaluating the patient proceeds smoothly, even though the steps are not always necessarily performed in the same order. These steps include the following:
A pin (Wartenberg) wheel was once a favorite tool of many neurologists because it was easy to use for sensory (pinprick) testing. Unless it is disposable (commercially available), this wheel is no longer recommended because of the risk of transmitting infection. The use of sterile safety pins (to be discarded after each use) is recommended.
Higher functions include gait, speech, and mental status. [8] These are referred to as higher functions because human bipedal gait, receptive and expressive speech, and cognitive function are more sophisticated than similar functions of any other member of the animal kingdom.
In hemiparesis, facial paresis may not be obvious. In mild cases, subtle features of facial paralysis (eg, flattening of the nasolabial fold on 1 side compared to the other, mild asymmetry of the palpebral fissures or of the face as the patient smiles) may be sought. The shoulder is adducted; the elbow is flexed; the forearm is pronated, and the wrist and fingers are flexed. In the lower extremities, the only indication of paresis may be that the ball of the patient's shoe may be worn more on the affected side.
In severe cases, the hand may be clenched; the knee is held in extension and the ankle is plantar flexed, making the paralyzed leg functionally longer than the other. The patient therefore has to circumduct the affected leg to ambulate.
In hemiplegic patients in whom all the paralysis is on the same side of the body, the lesion is of the contralateral upper motor neuron. In most cases, the lesion lies in the cortical, subcortical, or capsular region (therefore above the brainstem). In the alternating or crossed hemiplegias, CN paralysis is ipsilateral to the lesion, and body paralysis is contralateral. In such cases, CN paralysis is of the lower motor neuron type, and the location of the affected CN helps determine the level of the lesion in the brainstem. Therefore, paralysis of CN III on the right side and body paralysis on the left (Weber syndrome) indicates a midbrain lesion, whereas a lesion of CN VII with crossed hemiplegia (Millard-Gubler syndrome) indicates a pontine lesion, and CN XII paralysis with crossed hemiplegia (Jackson syndrome) indicates a lower medullary lesion.
In ataxia, the patient spreads his or her legs apart to widen the base of support to compensate for the imbalance while standing or walking. In severe cases, patients stagger as they walk. The heel-to-toe or tandem walking maneuvers and standing on 1 leg uncover subtle forms of ataxia.
Ataxia results from midline lesions of the cerebellum and may be isolated or associated with other cerebellar findings (see Cerebellar signs). When the lesion is unilateral, the patient may veer to the side of the lesion. With bilateral cerebellar involvement, the patient may fall to either side.
The individual takes short steps to the point of practically not moving forward or making little progress. In other words, the patient appears to shuffle his or her legs rather than put them forward. In some patients, the steps (albeit short) and pace may vary with a tendency for the patient to accelerate (festinating gait) as he or she walks. Both types are seen in Parkinson disease and may be associated with other extrapyramidal signs.
In steppage (high-stepping, slapping), the individual takes high steps as if climbing a flight of stairs while walking on a level surface. This peculiar gait pattern results from the patient trying to avoid injury to the feet (from dragging them) by stepping high. However, as the patient puts the feet down 1 by 1, they slap the ground, hence the description of a foot-slapping gait. This is 1 condition that can be diagnosed even before the patient enters the room because the sound is so characteristic.
In this condition, the legs are held in adduction at the hip and the thighs rub against each other as the patient walks. Spasm of the inner thigh muscles also occurs. If the spasm is severe, with each advancing step the knees tend to slide over each other like the blades of a pair of scissors. This is typically seen in cerebral diplegia, a form of cerebral palsy.
The most frequent cause of this problem is the common cold, which results in dysphonia due to inflammation of the larynx. Dysphonia may also occur in patients with hypothyroidism, as a result of thickening of the vocal cords from amyloid deposits. Neurologic causes include unilateral recurrent laryngeal nerve paralysis and lesions of the vagus nerve. Intermittent hoarseness may affect patients with vagus nerve stimulator implants, which are used for the treatment of certain medically intractable forms of epilepsy (MIE) and pharmacoresistent depression (PRD).
Dysarthria is the inability to articulate spoken words. The quality of oration is impaired, but the content remains intact (eg, slurred speech). The patient's ability to understand and synthesize speech remains intact. It results from paralysis of pharyngeal, palatal, lingual, or facial musculature. It also is observed with cerebellar lesions and/or disease (eg, scanning or staccato speech).
In dysphasia, the ability to process language is impaired, resulting in an inability to understand (ie, receptive or sensory or Wernicke aphasia), transfer signals from the Wernicke to the Broca area (ie, conduction aphasia), or properly execute speech (ie, expressive, motor, or Broca aphasia). The combination of Broca and Wernicke aphasias is referred to as global aphasia.
Another function that is impaired in all 4 of the aphasias mentioned above is repetition. This finding is important in the diagnosis of transcortical aphasias. When repetition is preserved in a patient with Broca aphasia, it signifies transcortical motor aphasia, and the lesion is anterior to the Broca area. When repetition is preserved in Wernicke aphasia, it is called transcortical sensory aphasia, and the lesion is posterior to the Wernicke area. Transcortical mixed aphasia and global aphasia are similar except for the preservation of repetition, and results from combined lesions anterior to the Broca and Wernicke areas, respectively.
Mental status evaluation includes testing of memory, orientation, intelligence, and the other aspects of the patient's psychic state. Only the first 3 are discussed here. When overt symptoms or signs of a psychic disturbance are present, psychiatric evaluation should be considered.
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