Clinical Director, University of Texas Medical Branch School of Medicine
Pain arising from the cervical part of the spine is felt in the neck and back of the head and may be projected to the shoulder and upper arm; it is evoked or enhanced by certain movements or positions of the neck and is accompanied by limitation of motion of the neck and by tenderness to palpation over the cervical spine pain treatment for sciatica order azulfidine 500mg mastercard. Pain of brachial plexus origin is experienced in the supraclavicular region pain treatment center brentwood buy cheap azulfidine 500 mg line, or in the axilla and around the shoulder; it may be worsened by certain maneuvers and positions of the arm and neck (extreme rotation) and is sometimes associated with tenderness of structures above the clavicle sciatica pain treatment exercise 500mg azulfidine mastercard. A palpable abnormality above the clavicle may disclose the cause of the plexopathy (aneurysm of the subclavian artery pain treatment centers of america buy azulfidine line, tumor, cervical rib). The combination of circulatory abnormalities and signs referable to the medial cord of the brachial plexus is characteristic of the thoracic outlet syndrome, described further on. Shoulder pain, like spine and plexus pain, may radiate into the arm and rarely into the hand, but sensorimotor and reflex changes- which always indicate disease of nerve roots, plexus, or nerves- are absent. In most patients the pain subsides gradually with immobilization and analgesics, followed by a program of increasing shoulder mobilization. If it does not, the injection of small amounts of corticosteroids into the bursa, or the site of major pain indicated by passive shoulder movement in the case of rotator cuff injuries, is often temporarily effective and allows the patient to mobilize the shoulder. Osteoarthritis and osteophytic spur formation of the cervical spine may cause pain that radiates into the back of the head, shoulders, and arm on one or both sides. Coincident compression of nerve roots is manifest by paresthesias, sensory loss, weakness and atrophy, and tendon reflex changes in the arms and hands. Pain in the neck may project into and cause numbness or burning of one half the tongue (the "neck-tongue syndrome"; see page 165). There may be difficulty in distinguishing cervical spondylosis with root and spinal cord compression from a primary neurologic disease (syringomyelia, amyotrophic lateral sclerosis, or tumor) with an unrelated cervical osteoarthritis, particularly at the C5-C6 and C6-C7 levels. A combination of osteoarthritis of the cervical spine with injury to ligaments and muscles when the neck has been forcibly extended and flexed. The injury ranges from a minor sprain of muscles and ligaments to severe tearing of these structures, to avulsion of muscle and tendon from vertebral body, and even to vertebral and intervertebral disc damage. Milder degrees of whiplash injury are often complicated by psychologic and compensation factors (see LaRocca for a review of this subject). Spinal rheumatoid arthritis may be restricted to the cervical apophysial (facet) joints and the atlantoaxial articulation. The usual manifestations are pain, stiffness, and limitation of motion in the neck and pain in the back of the head. In contrast to ankylosing spondylitis, rheumatoid arthritis is rarely confined to the spine. Because of major affection of other joints, the diagnosis is relatively easy to make, but significant involvement of the cervical spine may be overlooked in patients with diffuse disease. In the advanced stages of the disease, one or several of the vertebrae may become displaced anteriorly, or a synovitis of the atlantoaxial joint may damage the transverse ligament of the atlas, resulting in forward displacement of the atlas on the axis, i. In either instance, serious and even life-threatening compression of the spinal cord may occur gradually or suddenly. Cautiously performed lateral radiographs in flexion and extension are useful in visualizing atlantoaxial dislocation or subluxation of the lower segments. Occipital headache and neck pain related to degenerative changes in the upper cervical facets is discussed with other cranial pains on page 164 (so-called third occipital nerve pain). Cervical Disc Herniation (Table 11-1) A common cause of neck, shoulder, and arm pain is disc herniation in the lower cervical region; the process is comparable to disc herniation in the lumbar region but gives rise, of course, to a different set of symptoms (Table 11-1). It appears most often without a clear and immediate cause, but it may develop after trauma, which may be major or minor (from sudden hyperextension of the neck, falls, diving accidents, forceful manipulations). The roots most commonly involved are the seventh (in 70 percent of cases) and the sixth (20 percent); fifth- and eighth-root involvement makes up the remaining 10 percent (Yoss et al). When the protruded disc lies between the sixth and seventh vertebrae, there is involvement of the seventh cervical root as outlined in Table 11-1. The pain is in the region of the shoulder blade, pectoral region and medial axilla, posterolateral upper arm, elbow and dorsal forearm, index and middle fingers, or all the fingers. Tenderness is most pronounced over the medial aspect of the shoulder blade opposite the third to fourth thoracic spinous processes and in the supraclavicular area and triceps region. Paresthesias and sensory loss are most evident in the second and third fingers or may be experienced in the tips of all the fingers.
There may be subdural effusions and mass effect pain medication for dogs metacam cheap azulfidine 500mg amex, either on the cerebral convexities gum pain treatment remedies order azulfidine visa, temporal lobes jaw pain treatment medications generic 500mg azulfidine overnight delivery, optic chiasm groin pain treatment exercises azulfidine 500mg generic, or cerebellar tonsils. Using ultrasound, Chen and colleagues have also described an enlarged superior ophthalmic vein and increased blood flow velocity in this vessel, both of which normalize after successful treatment. Rarely, a case of intracranial hypotension becomes chronic; the headache is then no longer responsive to recumbency. Reference has already been made to this syndrome and to the slit ventricles in children who have been treated for hydrocephalus. Usually the valve setting is too low, and readjustment to maintain a higher pressure is corrective. At least 75 percent of patients are thus relieved of the headache, according to Safa-Tisseront and colleagues; they report that after a second injection, improvement is effected in 97 percent. Many patients have transient back or radicular pain (sciatica) following the blood patch. Curiously, the headache is often relieved almost immediately even if the blood is injected at some distance from the original puncture (although the procedure is usually done at the same level as the previous spinal tap). Moreover, the volume of blood injected, usually about 20 mL, is not related to the chances of success. The mechanism of this rapid improvement may not simply be the plugging of a dural leak. A number of patients fail to benefit or have only transient effects; it is then unclear whether repeating the procedure is helpful. The administration of caffeine-ergotamine preparations or intravenous caffeine may also have a salutary though temporary effect on the headache. The addition of analgesic medication is required if the patient must get up to care for himself or to travel. In protracted cases, patience is called for, since most headaches will resolve in 2 weeks or less. As to mechanism, Panullo and colleagues have shown that there is a downward displacement of the upper brainstem and posterior fossa contents when the patient assumes the upright position; but, as pointed out in Chap. These give rise to some of the most intractable low-pressure syndromes and must be investigated by radiologic and nuclide studies in order to establish the site of leakage. Several such leaks in our experience have been intermittent, adding to the difficulty in diagnosis. The point being made here is that these structures may also be involved in a number of noninfective processes, some of obscure origin. The lower spinal roots or spinal cord alone may be implicated in "spinal arachnoiditis. This may be accompanied by a pachymeningitis, and the latter may also be restricted to the cervical dura, also discussed below. A predominant localization to these basal or cervical structures may be apparent even in cases of diffuse cerebrospinal meningeal reactions, perhaps because of an uneven concentration of the noxious agent. In other instances, the primary disease appears to have arisen in the dura, with extension only to the adjacent piaarachnoid. In yet other instances, the ependyma of the aqueduct or fourth ventricle is primarily involved. The mechanisms by which these meningeal reactions affect parenchymal structures (brain, cord, and nerve roots) are not fully understood. Progressive constriction of nerve roots and spinal cord, literally a strangulation of these structures, is another plausible mechanism, but it is difficult to separate vascular factors from mechanical ones. Since any toxic agent introduced into the subarachnoid space has free access, via VirchowRobin spaces, to the superficial parts of the brain and spinal cord, direct parenchymal injury may follow. Perivascular reactions of subpial vessels, as in infectious processes, would be a plausible mechanism of injury to optic nerves and spinal cord, where long stretches of myelinated fibers abut the pia. Regional Arachnoiditis Arachnoiditis limited to the lumbosacral roots has followed ruptured discs, myelograms, and spinal surgery. Usually, there is sciatica and chronic neuropathic pain in the back and lower extremities, but sensorimotor and reflex changes in the legs are variable. The etiologic factors have been singularly elusive although in the past it followed the instillation of iophendylate (Pantopaque) for myelography and corticosteroids (for pain or multiple sclerosis) and other irritative agents.
The intermediate position of the limbic structures enables them to transmit neocortical effects from their outer side to the hypothalamus and midbrain on their inner side treatment for dog neck pain azulfidine 500mg for sale. The role of the cingulate gyrus in the behavior of animals and humans has been the subject of much discussion blue ridge pain treatment center order azulfidine 500mg online. Stimulation is said to produce autonomic effects similar to the vegetative correlates of emotion (increase in heart rate and blood pressure pain treatment back purchase azulfidine 500 mg with mastercard, dilatation of pupils pain treatment for uti generic 500 mg azulfidine amex, piloerection, respiratory arrest, breath-holding). More complex responses such as fear, anxiety, or pleasure have been reported during neurosurgical stimulative and ablative procedures, although these results are inconsistent. Bilateral cingulectomies performed in psychotic and neurotic patients result in an overall diminution of emotional reactions (Ballantine et al; Brown). Some investigators believe that the cingulate gyri are also involved in memory processing (functioning presumably in connection with the mediodorsal thalamic nuclei and mediotemporal lobes) and in exploratory behavior and visually focused attention. In humans, this system appears to be more efficient in the nondominant hemisphere, according to Bear. Baleydier and Mauguiere emphasize this dual function- in cognition and in emotional reactions- of the cingulate gyrus. Another aspect of limbic function has come to light as information is being acquired about neurotransmitters. The concentration of norepinephrine is highest in the hypothalamus and next highest in the medial parts of the limbic system; at least 70 percent of this monoamine is concentrated in terminals of axons that arise in the medulla and in the locus ceruleus of the rostral pons. Axons of other ascending fibers- especially those originating in the reticular formation of the midbrain and terminating in the amygdala and septal nuclei as well as in lateral parts of the limbic lobe- are rich in serotonin. The axons of neurons in the ventral tegmental parts of the midbrain, which ascend in the medial forebrain bundle and the nigrostriatal pathway, contain a high content of dopamine. Emotional Disturbances in Hallucinating and Deluded Patients these are best portrayed by the patient with a florid delirium. Threatened by imaginary figures and voices that seem real and Table 25-1 Neurology of emotional disturbances I. We have seen a patient slash his wrists and another try to drown himself in response to hallucinatory voices that admonished them for their worthlessness and the shame they had brought on their families. But the abnormality in these circumstances is one of disordered perception and thinking, and we have no reason to believe that there is a derangement of the mechanisms for emotional expression. There also occurs a state- difficult to classify- of overwhelming emotionality in patients who are in severe acute pain. We have encountered this with spinal subdural hemorrhage, subarachnoid hemorrhage, explosive migraine, trauma with multiple fractures, and intense pelvic, renal, or abdominal pain, all understandable as responses to extralimbic stimuli. Table 25-2 Causes of pseudobulbar affective display Bilateral strokes (lacunes in the cerebral hemispheres or pons most often, and after several strokes in succession) Binswanger diffuse leukoencephalopathy (Chap. The degree to which this pertains varies with gender and ethnicity and has more to do with social norms than with biology. In the realm of neurologic disease, a patient whose cerebrum has been damaged- for example, by a series of vascular lesions- may suffer the humiliation of crying in public upon meeting an old friend or hearing the national anthem, or of displaying uncontrollable laughter in response to a mildly amusing remark or an attempt to tell a funny story. There may also be easy vacillation from one state to another, an emotional lability that has for more than a century been accepted as a sign of "organic brain disease. Perhaps lesions of the frontal lobes more than those of other parts of the brain are conducive to this state, but the authors are unaware of a critical clinicoanatomic study that substantiates this impression. Emotional lability is a frequent accompaniment of diffuse cerebral diseases such as Alzheimer disease, but these diseases, of course, also involve the limbic cortex. Also under this heading might be included the tearfulness and facile mood that so often accompany chronic diseases of the nervous system, and the shallow facetiousness (Witzelsucht) and behavioral disinhibition of the patient with frontal lobe disease. Pathologic (Pseudobulbar, Forced, Spasmodic) Laughing and Crying this form of disordered emotional expression, characterized by outbursts of involuntary, uncontrollable, and stereotyped laughing or crying, has been well recognized since the late nineteenth century. Numerous references to these conditions (the Zwangslachen and Zwangsweinen of German neurologists and the rire et pleurer spasmodiques of the French) can be found in the writings of Oppenheim, von Monakow, and Wilson (see Wilson for historical references). The term emotional incontinence applied by psychiatrists is perhaps accurate but a bit pejorative. Forced laughing and crying always has a pathologic basis in the brain, either diffuse or focal; hence this stands as a syndrome of multiple causes. It may occur with degenerative and vascular diseases of the brain (Table 25-2) and no doubt is the direct result of them, but often the diffuse nature of the underlying disease precludes useful topographic analysis and clinicoanatomic correlation. The best examples of pathologic laughing and crying are provided by lacunar vascular disease but also by amyotrophic lateral sclerosis, multiple sclerosis, and progressive supranuclear palsy, in each case the lesions being distributed bilaterally and generally involving the motor tracts, more specifically, the corticobulbar motor system, as discussed further on.
Hence cross-modal matching tasks (auditory-visual lower back pain treatment left side buy azulfidine cheap, visual-auditory treatment for post shingles nerve pain buy generic azulfidine, visual-tactile pain treatment center dr mckellar order generic azulfidine, tactile-visual pain medication for dogs advil purchase azulfidine 500 mg fast delivery, auditory-tactile, etc. Such patients can read and understand spoken words but cannot grasp the meaning of a sentence if it contains elements of relationship. The recognition and naming of parts of the body and the distinction of right from left and up from down are learned, verbally mediated spatial concepts that are disturbed by lesions in the dominant parietal lobe. If the lesion is small and predominantly cortical, optokinetic nystagmus is usually retained; with deep lesions, it is abolished, with the target moving ipsilaterally (see Chap. From time to time, severe left-sided visual neglect results from a lesion in the right angular gyrus (see Mort and colleagues). With posterior parietal lesions, as noted by Holmes and Horrax, there are deficits in localization of visual stimuli, inability to compare the sizes of objects, failure to avoid objects when walking, inability to count objects, disturbances in smooth-pursuit eye movements, and loss of stereoscopic vision. Cogan observed that the eyes may deviate away from the lesion on forced lid closure, a "spasticity of conjugate gaze"; we have been able to elicit this sign only rarely. Visual Disorientation and Disorders of Spatial (Topographic) Localization Spatial orientation depends on the integration of visual, tactile, and kinesthetic perceptions, but there are instances in which the defect in visual perception predominates. Patients with this disorder are unable to orient themselves in an abstract spatial setting (topographagnosia). Such patients cannot draw the floor plan of their house or a map of their town- or of the United States- and cannot describe a familiar route, as from home to work, for example, or find their way in familiar surroundings. This disorder is almost invariably caused by lesions in the dorsal convexity of the right parietal lobe, and it is separable from the anosognosia discussed earlier. A common and striking disorder of motor behavior of the eyelids is seen in many patients with large acute lesions of the right parietal lobe. This gives the erroneous impression that the patient is drowsy or stuporous, but it will be found that a quick reply is given to whispered questions. In more severe cases, the lids are held shut and opening is strongly resisted, to the point of making an examination of the pupils and fundi impossible. Auditory Neglect this defect in appreciation of the left side of the environment is less apparent than is visual neglect, but it is no less striking when it occurs. Many patients with acute right parietal lesions are initially unresponsive to voices or noises on the left side, but the syndrome is rarely persistent. Special tests, however, demonstrate, in many of these patients, a displacement of the direction of the perceived origin of sounds toward the left. This defect is separable from visual agnosia (see De Renzi et al); curiously, it may be worsened by the introduction of visual cues. Subtle differences between the allocation of spatial attention to sound (auditory neglect) and a distortion in its localization may be found in different cases, but the main lesion usually lies in the right superior lobule, and the same bias for left hemispheric lesions applies as for visual inattention. Corticosensory syndrome and sensory extinction (or total hemianesthesia with large acute lesions of white matter) B. Mild hemiparesis (variable), unilateral muscular atrophy in children, hypotonia, poverty of movement, hemiataxia (all seen only occasionally) C. Homonymous hemianopia or inferior quadrantanopia (incongruent or congruent) or visual inattention D. Abolition of optokinetic nystagmus with target moving toward side of the lesion E. Effects of unilateral disease of the dominant (left) parietal lobe (in right-handed and most left-handed patients)- additional phenomena include A. Gerstmann syndrome (dysgraphia, dyscalculia, finger agnosia, right-left confusion) C. Anosognosia, dressing and constructional apraxias (these disorders may occur with lesions of either hemisphere but one observed more frequently and are of greater severity with lesions of the nondominant one) D. Visual spatial imperception, spatial disorientation, and complete or partial Balint syndrome (optic apraxia, described below) With all these parietal syndromes, if the disease is sufficiently extensive, there may be a reduction in the capacity to think clearly as well as inattentiveness and slightly impaired memory. It is still not possible to present an all-embracing formula of parietal lobe function. In this way, parietal lesions cause disorders of specific types of self-consciousness or self-awareness that are tied to sensory modalities, but they do not do so in the fundamental way that results from lesions of the temporal lobe. And, as Hubel and Wiesel have shown, the response patterns of neurons in both occipital lobes to edges and moving visual stimuli, to onand-off effects of light, and to colors are much different from what was originally supposed.
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