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Knowledge of the motor and sensory innervation of the peripheral nerve in question is needed for a satisfactory diagnosis. It is not practical to memorize the precise sensorimotor distribution of each peripheral nerve, and special manuals, such as Aids to the Examination of the Peripheral Nervous System, should be consulted (see also Table 46-1). In addition, it is important to decide whether the lesion is a temporary one of electrical conduction alone or whether there has been a structural interruption of nerve fibers, requiring nerve regeneration or corrective surgery for recovery. If there is no evidence of upper or lower motor neuron disease but certain movements are nonetheless imperfectly performed, one should look for a disorder of position sense or cerebellar coordination or for rigidity with abnormalities of posture and movement due to disease of the basal ganglia (Chap. In the absence of these disorders, the possibility of an apraxic disorder should be investigated by the methods outlined earlier. Hysterical Paralysis Hysterical paralysis may involve one arm or leg, both legs, or all of one side of the body. Tendon reflexes are retained and atrophy is lacking in hysterical paralysis, features that distinguish it from chronic lower motor neuron disease. Diagnostic difficulty arises only in certain acute cases of upper motor neuron disease that lack the usual changes in reflexes and muscle tone. Sometimes there is loss of sensation in the paralyzed parts and loss of sight, hearing, and smell on the paralyzed side- a pattern of sensory changes that is never seen in organic disease of the nervous system. When the hysterical patient is asked to move the affected limbs, the movements tend to be slow, hesitant, and jerky, often with contraction of agonist and antagonist muscles simultaneously and intermittently ("give-way" weakness). Lack of effort is usually obvious, despite facial and other expressions to the contrary. The weakness is inconsistent; some movements are performed tentatively and moments later another movement involving the same muscles is performed naturally. With organic hemiplegia, downward pressure will be felt from the nonparalyzed leg. The examiner then removes his hand from under the nonparalyzed leg, places it on top of the nonparalyzed one, and asks the patient to raise that leg. In true hemiplegia, no added pressure will be felt by the hand that remained beneath the heel of the paralyzed leg. Or, more useful in our experience, the normal leg fails to demonstrate downward pressure when the hysteric is asked to elevate the supposedly paralyzed one, thereby indicating a lack of voluntary effort. In the patient with organic hemiplegia, there is an involuntary flexion of the paretic lower limb; in paraplegia, both limbs are flexed as the trunk is flexed; in hysterical hemiplegia, only the normal leg may be flexed; and in hysterical paraplegia, neither leg is flexed. Muscular Paralysis and Spasm Unattended by Visible Changes in Nerve or Muscle A discussion of motor paralysis would not be complete without some reference to a group of diseases in which muscle weakness may be profound but there are no overt structural changes in motor nerve cells or nerve fibers. Almost any disease of the neuromus cular junction and many diseases of muscle may cause this combination. This group comprises myasthenia gravis; inflammatory myopathies, the muscular dystrophies, and myotonia congenita (Thomsen disease); familial periodic paralysis; disorders of potassium, sodium, calcium, and magnesium metabolism; tetany; tetanus; poisoning by Clostridium botulinum; black widow spider bite; and the thyroid and other endocrine myopathies. In these diseases, each with a fairly distinctive clinical picture, the abnormality is essentially biochemical; their investigation requires special biochemical and histochemical tests and electron microscopic study. These subjects are discussed in the sections on muscle disease later in this book. They are believed, on good evidence, to be an expression of the extrapyramidal motor system, meaning- according to S. Wilson, who introduced this term- the motor structures of the basal ganglia and certain related thalamic and brainstem nuclei. In health, the activities of the basal ganglia and the cerebellum are blended with and modulate the corticospinal and corticalbrainstem-spinal systems. The static postural activities of the former are indispensable to the voluntary movements of the latter. The close association of the basal ganglia and corticospinal systems becomes evident in the course of many forms of neurologic disease. Cerebral lesions that involve the corticospinal tracts result not only in a contralateral paralysis of volitional movements but also in a fixed posture or attitude in which the arm is flexed and the leg extended (predilection of Wernicke-Mann or hemiplegic dystonia of Denny-Brown). In these released motor patterns, one has evidence of labyrinthine, tonic neck, and other postural reflexes that are mediated through nonpyramidal bulbospinal and other brainstem motor systems. Nevertheless, this division remains a useful if not an essential concept in clinical work, since it compels a distinction between several motor syndromes- one that is characterized by a loss of volitional movement accompanied by spasticity; a second by akinesia, rigidity, and tremor without loss of voluntary movement; a third by involuntary movements (choreoathetosis and dystonia); and yet another by incoordination (ataxia). The clinical differences between corticospinal and extrapyramidal syndromes are summarized in Table 4-1.

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Often, as the deficit recedes, the arm becomes involved by athetotic, tremulous, or ataxic movements; there may be an interval of months or years between the hemiplegia and the athetosis. Encephaloclastic (destructive) lesions underlie most of the cases of infantile hemiplegia and some cases of bilateral hemiplegia (as well as many cases of seizures in the first few days of life). Precipitant delivery, fetal distress, and prepartum uterine hemorrhage may have been indications of the process. The lesions seemingly reflect those of circulatory insufficiency (ischemia), the result of hypotension or local circulatory failure. What is most notable is that the ischemia tends to affect the tissues lying in arterial cortical border zones; there may also be venous stasis with congestion and hemorrhage occurring particularly in the deep central structures, such as the basal ganglia and periventricular matrix zones. There is severe encephalomalacia mainly in the territory of the right middle cerebral artery. The quadriplegic state differs from bilateral hemiplegias in that the bulbar musculature is often involved in the latter and mental retardation is more severe. The condition is relatively rare and is usually due to a bilateral cerebral lesion. However, one should also be alert to the possibility of a high cervical cord lesion. In the infant, this is usually the result of a fracture dislocation of the cervical spine incurred during a difficult breech delivery. Similarly, in paraplegia, with weakness or paralysis limited to the legs, the lesion may be either a cerebral or a spinal one. Sphincteric disturbances and a loss of somatic sensation below a certain level on the trunk always point to a spinal localization. Congenital cysts, tumors, and diastematomyelia are more frequently causes of paraplegia than of quadriplegia. Another recognized cause of infantile paraplegia is spinal cord infarction from thrombotic complications of umbilical artery catheterization. Extrapyramidal Syndromes the spastic cerebral diplegias discussed above shade almost imperceptibly into the congenital extrapyramidal syndromes. Patients with the latter syndromes are found in every cerebral palsy clinic, and ultimately they reach adult neurology clinics as well. Corticospinal tract signs may be completely absent, and the student, familiar only with the syndrome of pure spastic diplegia, is always puzzled as to their classification. Some cases of extrapyramidal type are undoubtedly attributable to severe perinatal hypoxia and others to diseases such as erythroblastosis fetalis with kernicterus. Double Athetosis this is probably the most frequent of the congenital extrapyramidal disorders. In our clinical material and in reported series of cases, two types stand out- one that is due to hyperbilirubinemia or Rh incompatibility (kernicterus, see below) and the other due to hypoxic-ischemic encephalopathy. With control of neonatal hyperbilirubinemia (by use of anti-Rh immune globulin, exchange transfusions, and phototherapy), kernicterus has almost disappeared, whereas the other, more severe hypoxicischemic form regularly continues to be seen. Rarely, a congenital, nonhemolytic icterus or a glucose-6-phosphate dehydrogenase deficiency produces the same syndrome. Like the spastic states, double athetosis may not be recognized at birth but only after several months or a year has elapsed. In some cases the appearance of choreoathetosis is for unexplained reasons delayed for several years; it may seem to progress during adolescence and even early adult life. It must then be differentiated from some of the inherited metabolic and degenerative extrapyramidal diseases. Chorea and athetosis dominate the clinical picture, but bewildering combinations of involuntary movements- including dystonia, ataxic tremor, myoclonus, and even hemiballismus- may be found in a single case. At times, we have been unable to classify the movement disorder because of its complexity.

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The pathophysiology of the spasm is believed to be focal demyelination nerve root compression. The demyelinated axon is theorized to activating adjacent nerve fibers by ephaptic transmission ("artificial" synapse of Granit et al). Another possible source of the spasm is spontaneous ectopic excitation arising in injured fibers. Nielsen and Jannetta have shown that ephaptic transmission disappears after the nerve is decompressed. Treatment Surgical decompression of a vascular loop, which involves exploration of the posterior fossa, carries some small risk. Another complication has been deafness due to injury of the adjacent eighth nerve. Also, there is a modest risk of recurrence of the spasms, usually within 2 years of the operation (Piatt and Wilkins). The authors suggest that patients with idiopathic hemifacial spasm should first be treated medically. Alexander and Moses noted that carbamazepine (Tegretol) in a dosage of 600 to 1200 mg/day controlled the spasm in two thirds of the patients. Some patients cannot tolerate these drugs, have only brief remissions, or fail to respond; they may be treated with botulinum toxin injected into the orbicularis oculi and other facial muscles. The hemifacial spasms are relieved for 4 to 5 months and injections can be repeated without danger. Some patients have been injected repeatedly for more than 5 years without apparent adverse effects. Other Disorders of the Facial Nerve Facial myokymia is a fine rippling activity of all the muscles of one side of the face mentioned above. The fibrillary nature of the involuntary movements and their arrhythmicity tend to distinguish them from the coarser intermittent facial spasms and contracture, tics, tardive dyskinesia, and clonus. Demyelination of the intrapontine part of the facial nerve and possibly supranuclear disinhibition of the facial nucleus have been the postulated mechanisms. A clonic or tonic contraction of one side of the face may be the sole manifestation of a cerebral cortical seizure. Involuntary recurrent spasm of both eyelids (blepharospasm) may occur with almost any form of dystonia but is most frequent in elderly persons as an isolated phenomenon, and there may be varying degrees of spasm of the other facial muscles (see page 93). Relaxant and tranquilizing drugs are of little help in this disorder, but injections of botulinum toxin into the orbicularis oculi muscles give temporary or lasting relief. A few of our patients have been helped (paradoxically) by L-dopa; baclofen, clonazepam, and tetrabenazine in increasing doses may be helpful. In the past, failing these measures, the periorbital muscles were destroyed by injections of doxorubicin or surgical myectomy (Hallett and Daroff). With the advent of botulinum treatment, there is no longer a need to resort to these extreme measures. Rhythmic unilateral myoclonia, akin to palatal myoclonus, may be restricted to facial, lingual, or laryngeal muscles. The Ninth, or Glossopharyngeal, Nerve Anatomic Considerations this nerve arises from the lateral surface of the medulla by a series of small roots that lie just rostral to those of the vagus nerve. The glossopharyngeal, vagus, and spinal accessory nerves leave the skull together through the jugular foramen and are then distributed peripherally. The ninth nerve is mainly sensory, with cell bodies in the inferior, or petrosal, ganglion (the central processes of which end in the nucleus solitarius) and the small superior ganglion (the central fibers of which enter the spinal trigeminal tract and nucleus). Within the nerve are afferent fibers from baroreceptors in the wall of the carotid sinus and from chemoreceptors in the carotid body. The baroreceptors are involved in the regulation of blood pressure, and chemoreceptors are responsible for the ventilatory responses to hypoxia. The somatic efferent fibers of the ninth nerve are derived from the nucleus ambiguus, and the visceral efferent (secretory) fibers, from the inferior salivatory nucleus. These fibers contribute in a limited way to the motor innervation of the striated musculature of the pharynx (mainly of the stylopharyngeus, which elevates the pharynx), the parotid gland, and the glands in the pharyngeal mucosa. It is commonly stated that this nerve mediates sensory impulses from the faucial tonsils, posterior wall of the pharynx, and part of the soft palate as well as taste sensation from the posterior third of the tongue. However, an isolated lesion of the ninth cranial nerve is a rarity, and the effects are not fully known.

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Weakness is minimal, and the tendon reflexes, although diminished, may be retained early in the course of the illness. Pain and thermal sense are reduced more than tactile, vibratory, and position sense (a "pseudosyringomyelic") pattern. Autonomic involvement is another important characteristic- loss of pupillary light reflexes and miosis, anhidrosis, vasomotor paralysis with orthostatic hypotension, alternating diarrhea and constipation, and impotence. Difficulty in walking also develops and has its basis in a combination of faulty position sense and mild muscle weakness. Cranial nerve involvement (facial weakness and numbness, loss of taste) is a late manifestation and occurs in only a few cases. A few patients have had severe amyloid heart disease from the onset (Ikeda et al). Weight loss may be pronounced, owing to anorexia and disordered bowel function and the later development of a malabsorption syndrome. Vitreous opacities (veils, specks, and strands) may progress to blindness, but this has been rare; in a few, there has been an impairment of hearing. In this and the following most common familial amyloidoses, the amyloid is derived from an inherited abnormality of serum protein transthyretin (formerly called "prealbumin"). In the originally described Andrade type, methionine replaces valine at amino acid 30; this has therefore been referred to as transthyretin amyloidosis. Familial amyloidosis with carpal tunnel syndrome (Swiss type) Falls and coworkers in 1955 and later Rukavina and associates described a large group of patients of Swiss stock living in Indiana who developed, in their fourth and fifth decades, a characteristic syndrome of acroparesthesias in the hands due to deposition of amyloid in the connective tissues and beneath the carpal ligaments. There was sensory loss and atrophic muscle weakness in the distribution of the median nerves, which were compressed. In some of the patients, other nerves of the arms were said to have become involved later. As with the Portuguese type, an abnormal transthyretin is the basis of the deposition of amyloid. Iowa type In 1969, van Allen described an Iowa kindred with onset, in their 30s, of a fairly severe sensorimotor neuropathy, involving the legs and then the arms. There was amyloid deposition in the testes, adrenal glands, and kidneys (the usual cause of death) as well as a high incidence of peptic ulcer disease. The amyloid in this disease is derived from apolipoprotein A-1, in which there is an amino acid substitution. Cranial neuropathy with corneal lattice dystrophy this unusual form of amyloid neuropathy was first described in three Finnish families by Meretoja- hence the label "Finnish type. Peripheral neuropathy may not be evident until the fifth decade, at which time the facial nerves, particularly their upper branches, become affected. The nerves of the limbs are involved even later and to a much lesser extent than in other amyloid neuropathies. In advanced cases there is a distinctive appearance of excessive skin folds about the face, facial diparesis, dysarthria, spasticity, and dense loss of posterior column function. At postmortem examination, deposits of amyloid are found in virtually every organ, but mainly in the kidneys and blood vessels and in the perineurium of affected nerves. The latter is normally an actin-binding protein, but it is also an important constituent of basement membranes, which may explain the deposition of amyloid in the cornea and skin. Diagnosis When the characteristic painful small-fiber type of sensory disturbance and autonomic changes are coupled with a family history of the same constellation, the diagnosis is not difficult. As noted in the earlier section on the acquired paraproteinemic neuropathy, the presence of a monoclonal (rarely polyclonal) immunoglobulin in the blood is found in only a limited number of patients with familial amyloid cases and it is of a low quantity, usually just above the upper limit of normal for the immunoglobulin subclass. Otherwise, as noted by several authors, the two types of amyloid disease are quite similar and, indeed, about 10 percent of cases thought to be acquired will in the end be found to have the genetic disorder (Lachmann et al). The situation has been rectified to some extent by the availability of gene sequencing to detect mutations related to amyloid. Such testing is justified if there is a low concentration paraprotein (or none) and a typical amyloidotic polyneuropathy and when the family history does not point to the correct diagnosis.

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The accompanying electrical form of an individual fasciculation potential is relatively constant. Fasciculation potentials are evidence of motor nerve fiber irritability, most often the result of reinnervation following nerve or motor neuron damage. Thus, the combination of fibrillations and fasciculations indicates active denervation combined with more chronic reinnervation of muscle; i. Other physiologic and pharmacologic evidence pointed to the first segment of the motor axon, or to the distal axon, or even to the motor point (the site of insertion of the nerve into muscle), involving elements of the postsynaptic muscle membrane (particularly in the case of benign fasciculations) as the source of the spontaneous electrical activity. It seems that several regions of the axon are capable of spontaneous impulse generation, depending on the underlying disease. Occasional fasciculation potentials- particularly in the calves, hands, and periocular or paranasal muscles- occur in many normal persons. They can be almost constant for days or weeks on end, or even for years in some individuals, without weakness or wasting; therefore they need not be taken as evidence of disease (benign fasciculations). Certain quantitative features of fasciculations, such as brief duration and a consistent pattern and location of firing, favor benign over pathologic discharges. Shivering induced by low temperature and twitchings associated with low serum calcium levels are other forms of fasciculatory activity. They are seen often in the early stages of poliomyelitis but only occasionally in the chronic phase of the disease, perhaps because the affected cells die rapidly. When anterior horn cells degenerate once again in older individuals who had had poliomyelitis (postpolio syndrome), fasciculations may return. Occasionally, they are seen in one muscle as a result of a compressive anterior root lesion, such as those caused by a protruded intervertebral disc; large numbers of axons may be affected, with the result that the fasciculations (or even cramps) may be more prominent than with disease of anterior horn cells. Fasciculation potentials in lesser numbers are also observed with chronic nerve entrapments. In all these cases, the damaged neuron or its axon seems to leave intact axons in a state of hyperirritability. The blocking of axon conduction by local anesthesia does not abolish the fasciculation, but curare-like drugs do so. The small motor unit discharges may occur singly or as doublets, triplets, or multiplets. The site of generation of this activity has also been contested, possibly because it may arise from several sites, but always the site is peripheral, not central, and is believed to correspond to an alteration in the calcium concentration in the microenvironment of the motor axon. Spontaneous discharges arising in large myelinated fibers have been implicated in the genesis of myokymia; indeed, demyelinating polyneuropathies are among the conditions that give rise to this phenomenon. Myokymia is also caused by peripheral nerve hyperexcitability due to both potassium channel mutations and antibodies against the channels. This activity may be blocked by lidocaine infusion around the peripheral nerve and may be diminished by carbamazepine or phenytoin. Focal and segmental myokymias differ in small ways from the generalized form of myokymia with regard to the timing and du- ration of the discharges. Segmental myokymia is a common occurrence in radiation injuries of the brachial plexus. The origin of these discharges (also referred to as neuromyotonia) is probably in the distal peripheral nerve, where activity of afferent fibers, possibly via ephaptic transmission, irregularly excites distal motor terminals. Segmental myokymia refers to similar activity in the distribution of one or more adjacent motor roots. The phenomenon of myotonia, which denotes a failure of voluntary relaxation of muscle because of sustained firing of the muscle membrane (see pages 1265 and 1270), is characterized by highfrequency repetitive discharges generally having a positive sharp waveform. These myotonic discharges wax and wane in amplitude and frequency, producing a "dive-bomber" sound on the audio monitor. The discharges can be elicited mechanically by percussion of the muscle or movement of the needle electrode and are also seen following voluntary contraction or electrical stimulation of the muscle via its motor nerve. If the muscle is activated repeatedly at short intervals, the late discharge becomes briefer and briefer and eventually disappears (see. The five lines are a continuous record of activity in the biceps brachii following a tap on the tendon. The initial response is within normal limits, but it is followed by a prolonged burst of rapid activity, gradually subsiding over a period of many seconds or minutes.

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Consumption Consumption: as clot is formed and then broken down or lost there is a constant consumption of clotting factors and platelets which will inevitably result in a potential deficiency of certain essential clotting elements. This is often used as the explanation for the common heard expression "the first clot is the best clot". In other words, the first time that the body attempts to form a clot, the combination of elements required for clotting and the bodily environment is closest to perfect and after that the conditions are never quite so ideal. An essential part is clearly to maintain as close to normal physiology as possible and we should go to considerable lengths to keep the casualty as warm as possible. As a result, we can have all of the key elements necessary for clotting and we can even supplement them. Acidosis results from poor perfusion and cold which both develop in shock as the blood pressure falls and circulation is lost or diverted away from non-essential tissues. However, throughout this period of low blood pressure there will be tissue underperfused resulting in a worsening acidosis. Such an acidosis will inevitably result in a worsening coagulopathy and ultimately an increased mortality. As such we must seek a compromise and a balance between increasing bleeding with more blood pressure and worsening shock and coagulopathy with underperfusion and permissive hypotension. Speed in the resus room, in terms of triage, assessment and ongoing care and then speed in getting to theatre and to achieving surgical control of bleeding and ultimately to intensive care where we can restore blood pressure and homeostasis. We can also attempt to optimise the essential clotting agents by including them as part of our massive haemorrhage protocol. One such study published in 2005 looked at the problem of dilutional coagulopathy and suggested that this can be minimised or managed by adopting a ratio of 1-1. A later study published in J Trauma in 2007 identified that diagnosis of coagulopathy in intensive care is too late and difficult or impossible to control. This seems like a simple and easy to adopt solution until we consider any potential negative effects of such an approach and there is considerable evidence to suggest that there is a poor risk/benefit ratio, especially in the critically ill, with little improvement in outcome. This risk is further increased with high levels of packed red blood cell transfusion. Platelets There is a similar debate for platelets as they are obviously play an essential part in the clotting process and deficiency from consumption or dilution will potentially greatly impair clotting, but at what level does this become a problem? However, others simply suggest keeping the platelet count higher than 100 (x109/L). This obviously requires a blood test and a count, which is often delayed and of limited value in a clinical major bleed situation. Another reason for delay occur as a result of platelets being stored centrally in the Blood Transfusion Service, which will usually require an emergency transport to the hospital and a typical delay of at least half an hour. In view of this very real practical issue, many units have dropped platelets from the first Major Haemorrhage pack, unless the patient is already known or identified as thrombocytopaenic. Platelets are stored at room temperature which increases the potential risk of bacterial contamination. In 2011, following a National Canadian consensus meeting considering these concerns, they have adopted a more conservative approach to high ratio transfusions and consider it a better balance of benefit vs risk. Their current strategy is initially 6 units of blood with 3 unit of fresh frozen plasma (2:1 but quoted as 6:3 as given as a pack). Blood counts are taken early and then results used for the next round of transfusion. Fibrinogen supplementation is currently recommended in trauma when the plasma level falls below 1. Calcium Calcium is an essential co-factor in clotting and it also has a significant part to play in normal myocardial contractility and function. Fibrinogen We must also consider all the other factors and co-factors involved in the clotting process and typically in major trauma the fibrinogen levels fall to critically low levels 296 Calcium has not been recommended during massive transfusion in recent times, but the levels are likely to be low or bound in transfused components and as such, plasma levels can fall rapidly during massive transfusion. This is because of both consumption during clot formation, dilution and loss from resuscitation fluid and binding of calcium by citrate preservatives found in packs of red cells. Alternatively, if rapidly available blood sampling can be provided, then ionised calcium levels should be kept at a level greater than 1mmol/L.

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Metastases to the skull and dura can occur with any tumor that metastasizes to bone, but they are particularly common with carcinoma of the breast and prostate and with multiple myeloma. Metastatic tumors of the convexity of the skull are usually asymptomatic, but those at the base may implicate the cranial nerve roots or the pituitary body. Occasionally, a carcinoma metastasizes to the subdural surface and compresses the brain, like a subdural hematoma. Almost one-third of them originate in the lung and half this number in the breast; melanoma is the third most frequent source in most series, and the gastrointestinal tract (particularly the colon and rectum) and kidney are the next most common. Carcinomas of the gallbladder, liver, thyroid, testicle, uterus, ovary, pancreas, etc. Tumors originating in the prostate, esophagus, oropharynx, and skin (except for melanoma) almost never metastasize to the substance of the brain. From a somewhat different point of view, certain neoplasms are particularly prone to metastasize to the brain- 75 percent of melanomas do so, 57 percent of testicular tumors, and 35 percent of bronchial carcinomas, of which 40 percent are small-cell tumors (Posner and Chernik). According to those authors, the cerebral metastasis is solitary in 47 percent of cases, a somewhat higher figure than that observed in our practice and reported by others (see Henson and Urich). The metastatic tumors most likely to be single come from kidney, breast, thyroid, and adenocarcinoma of the lung. Generally the cerebral metastasis forms a circumscribed mass, usually solid but sometimes in the form of a ring. Often edema alone is evident on imaging studies until the administration of contrast exposes small tumor nodules. Metastases from melanoma and chorioepithelioma are often hemorrhagic, but some from the lung, thyroid, and kidney exhibit this characteristic as well. In a number of these cases, one-quarter in some series, the first manifestation of the metastasis is an intratumoral hemorrhage. The usual clinical picture of metastatic carcinoma of the brain is much like that of glioblastoma multiforme. Seizures, headache, focal weakness, mental and behavioral abnormalities, ataxia, aphasia, and signs of increased intracranial pressure- all inexorably progressive over a few weeks or months- are the common clinical manifestations. One that presents particular difficulty in diagnosis is a diffuse cerebral disturbance with headache, nervousness, depressed mood, trembling, confusion, and forgetfulness, resembling a relatively rapid dementia from degenerative disease. Cerebellar metastasis, with headache, dizziness, and ataxia (the latter being brought out only by having the patient walk) is another condition that may be difficult to diagnose. Brainstem metastases, most often originating in the lung, are rare but distinctive, giving rise to diplopia, imbalance, and facial palsy as in the characteristic case described by Weiss and Richardson. Infrequently, the onset of symptoms from brain metastases is relatively abrupt or even "stroke-like" rather than insidious. Some cases of sudden onset can be explained by bleeding into the tumor and others perhaps by tumor embolism, causing cerebral infarction with early regression of symptoms and later progression from the metastasis left in its wake. Also, nonthrombolic (marantic) endocarditis with cerebral embolism must be suspected when a stroke-like event occurs in a tumor patient. It is not unusual for one or other of these neurologic manifestations to precede those of the discovery of a pancreatic, bowel, gastric, breast, or lung carcinoma. When any of the several clinical syndromes due to metastatic tumor is fully developed, diagnosis is relatively easy. If only headache and vomiting are present, a common error is to attribute them to migraine or tension headache (page 158). One should invoke such explanations only if the patient has the standard symptoms of one of these conditions. Multiple nodular deposits of tumor in the brain on imaging studies most clearly distinguish metastatic cancer from other tumors but at the same time raise the possibility, on radiologic grounds, of brain abscesses. Solitary metastatic disease first must be distinguished from a primary tumor of the brain. Also, metastases must not be confused with certain neurologic syndromes that sometimes accompany carcinoma but are not due to the invasion or compression of the nervous system by tumor.

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The air is apparent as a very low density collection that compresses the frontal lobes. Depressed ("derby hat") fractures are of significance only if the underlying dura is lacerated or the brain is compressed by indentation of bone. Cerebral Concussion Mechanisms of Concussion Much has been written about the mechanisms of concussion and coma in closed, or blunt, head injury. Certain facts concerning these conditions stand out: (1) Concussion, meaning a reversible traumatic paralysis of nervous function, is always immediate (not delayed even by seconds). Admittedly, in the more prolonged states of coma, there is a greater chance of finding hemorrhage and contusion, which undoubtedly contribute to the persistence of coma and the likelihood of irreversible change. These two types of blunt (nonpenetrating) head injury are called accelerative and decelerative, respectively. The mechanism of concussive "cerebral paralysis" has been interpreted in various ways throughout medical history in light of the state of scientific knowledge at a particular period of time. The favored hypotheses for the better part of a century were "vasoparalysis" (suggested by Fischer in 1870) or an arrest of circulation by an instantaneous rise in intracranial pressure (proposed by Strohmeyer in 1864 and popularized by Trotter in 1932). Jefferson, in his essay on the nature of concussion (1944), convincingly refuted these vascular hypotheses. Later, Shatsky and coworkers, by the use of high-speed cineangiography, showed displacement of vessels but no arrest of circulation immediately after impact. Beginning with the work of Denny-Brown and Russell in 1941, the physical factors involved in head and brain injury have been subjected to careful analysis. These investigators demonstrated, in the monkey and cat, that concussion resulted when the freely moving head was struck by a heavy mass. If the head was prevented from moving at the moment of impact, the same degree of force invariably failed to produce concussion. More recently, the importance of head motion per se was verified by Gennarelli and colleagues, who were able to induce concussion in primates by rapid acceleration of the head without impact, a condition that rarely occurs in humans. Holbourn, a Cambridge physicist, from a study of gelatin models under conditions simulating head trauma, deduced that when the head is struck, movement of the partly tethered but suspended brain always lags (due to inertia); but inevitably the brain moves also, and when it does it must rotate, for it occupies a round skull whose motions (because of attachment to the neck) usually describe an arc. Pudenz and Sheldon and later Ommaya and coworkers (1974) proved the correctness of this assumption by photographing the brain through a transparent (Lucite) calvarium at the moment of impact. The brain is thus subjected to shearing stresses set up by rotational forces mainly in the sagittal plane centered at its point of tethering in the high midbrain and subthalamus. The torque at the level of the upper reticular formation would explain the immediate loss of consciousness, as described below. Also, these rotational movements of the brain provide a reasonable explanation for the occurrence of surface injuries in certain places, i. These views on the site and mechanism of concussion have been supported by a number of additional physiologic observations. Foltz and Schmidt, in 1956, suggested that the reticular formation of the upper brainstem was the anatomic site of concussive injury. They showed that in the concussed monkey, lemniscal sensory transmission through the brainstem was unaltered, but its effect in activating the high reticular formation was blocked. They also demonstrated that the electrical activity of the medial reticular formation was depressed for a longer time and more severely than that of the cerebral cortex. In 1956 and again in 1961, Strich described the neuropathologic findings in patients who died months after severe closed head injuries that had caused immediate and protracted coma. In all of her cases- in which there were no signs of skull fracture, raised intracranial pressure, or gross subarachnoid hemorrhage- she observed an uneven but diffuse degeneration of the cerebral white matter. In cases of shorter survival (up to 6 weeks), she observed ballooning and interruption of axis cylinders. Adams and colleagues, and by Gennarelli and coworkers, the last of these groups working with monkeys. Strich interpreted the extensive white matter lesions, both in the hemispheres and in the brainstem, to represent a degeneration of nerve fibers that had been stretched or torn by the shear stresses set up during rotational acceleration of the head (diffuse axonal injury), as had been postulated earlier by Holbourn. She suggested that if nerve fibers are stretched rather than torn, the lesions may be reversible and may play a part in the mechanism of concussion. Symonds elaborated this view and saw in the shearing stresses- which are maximal at the point where the cerebral hemispheres rotate on the relatively fixed brainstem.


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