Книги по МРТ КТ на английском языке / PLUM AND POSNER S DIAGNOSIS OF STUPOR AND COM-1

where her blood pressure was 180/100 mm Hg. She had sighing respirations, which shortly changed to a Cheyne-Stokes pattern. The pupils were 4 mm in diameter and unreactive to light. The oculocephalic responses were absent, but cold caloric irrigation induced abduction of the eye only on the side being irrigated. She responded to noxious stimuli with extensor posturing and occasionally was wracked by spontaneous waves of extensor rigidity.

CT scan was initially read as normal, and she was brought to the neurology intensive care unit. The CSF pressure on lumbar puncture was 140 mm of water; the fluid was clear, without cells, and contained 35 mg/dL of protein. Two days later, the patient continued in coma with extensor responses to noxious stimulation; the pupils remained fixed in midposition, and there was no ocular response to cold caloric irrigation. Respirations were eupneic. Repeat CT scan showed lucency in the medial pons and midbrain. The next day she died and the brain was examined postmortem. The basilar artery was occluded in its midportion by a recent thrombus 1 cm in length. There was extensive infarction of the rostral portion of the base of the pons, as well as the medial pontine and midbrain tegmentum. The lower portion of the pons and the medulla were intact.

Comment: This woman suffered an acute brainstem infarction with unusually symmetric neurologic signs. She was initially diagnosed with an infarct at the midbrain level based on her clinical picture. Other considerations included a thalamic hemorrhage with sudden acute transtentorial her-

niation producing a picture of acute midbrain transection. However, such rapid progression to a midbrain level almost never occurs in patients with supratentorial intracerebral hemorrhages. The CT scan and the absence of red blood cells on the lumbar puncture ruled out subarachnoid hemorrhage as well. Finally, the neurologic signs of midbrain damage in this patient remained nearly constant from onset, whereas transtentorial herniation would rapidly have produced further rostral-caudal deterioration.

Brainstem Hemorrhage

Relatively discrete brainstem hemorrhage can affect the midbrain,249 the pons,250 or the me-

dulla.251 The causes of brainstem hemorrhage include hypertension, vascular malformations, clotting disorders, or trauma. Hypertensive brainstem hemorrhages tend to lie deep within the brainstem substance, are rather diffuse, frequently rupture into the fourth ventricle, occur in elderly persons, and have a poor prognosis for recovery.252 Brainstem hematomas caused by vascular malformations occur in younger individuals, are usually subependymal in location, tend to be more discrete, do not rupture into the ventricle, and have a good prognosis for recovery. Surgery generally does not have a place in treating brainstem hypertensive hemorrhages, but it is sometimes possible to remove a vascular malformation, particularly a cavernous angioma.

Primary midbrain hemorrhages, which may be of either type, are rare. Most patients present acutely with headache, alterations of consciousness, and abnormal eye signs (Table 4–17). The diagnosis is obvious on imaging. Most patients recover completely from bleeds from cavernous angiomas; some remain with mild neurologic deficits.

Hemorrhage into the pons typically arises from the paramedian arterioles, beginning at the base of the tegmentum, and usually dissecting in all directions in a relatively symmetric fashion (Figure 4–9A). Rupture into the fourth ventricle is frequent, but dissection into the medulla is rare. Although most patients lose consciousness immediately, in a few cases (such as Patient 2–1) this is delayed, and in others when the hematoma is small, and particularly when it is confined to the base of the pons, consciousness can be retained. However, such patients often have other focal signs (e.g., a bleed into the base of the pons can present with an acute locked-in state). Such patients, however, often have considerable recovery.254

Coma caused by pontine hemorrhage begins abruptly, usually during the hours when patients are awake and active and often without a prodrome. When the onset is witnessed, only a few patients complain of symptoms such as sudden occipital headache, vomiting, dyscoordination, or slurred speech before losing consciousness.255 Almost every patient with pontine hemorrhage has respiratory abnormalities of the brainstem type: Cheyne-Stokes breathing, apneustic or gasping breathing, and progressive slowing of respiration or apnea250 (Table 4–18).

In patients who present in coma, the pupils are nearly always abnormal and usually pinpoint. The pupils are often thought to be fixed to light on initial examination, but close examination with a magnifying glass usually demonstrates further constriction. The ciliospinal response disappears. If the hemorrhage extends into the midbrain, pupils may become asymmetric or dilate to midposition. About onethird of patients suffer from oculomotor abnormalities such as skewed or lateral ocular deviations or ocular bobbing (or one of its variants), and the oculocephalic responses disappear. Motor signs vary according to the extent of the hemorrhage. Some subjects become diffusely rigid, tremble, and suffer repeated waves

of decerebrate rigidity. More frequently, however, patients are quadriplegic and flaccid with flexor responses at the hip, knee, and great toe to plantar stimulation, a reflex combination characteristic of acute low brainstem damage when it accompanies acute coma. Nearly all patients with pontine hemorrhage who survive more than

a few hours develop fever with body temperatures of 38.58C to 408C.256,257

The diagnosis of pontine hemorrhage is usually straightforward. Almost no other lesion, except an occasional cerebellar hemorrhage with secondary dissection into the brainstem, produces sudden coma with periodic or ataxic breathing, pinpoint pupils, absence of oculovestibular responses, and quadriplegia. The pinpoint pupils may suggest an opiate overdose, but the other eye signs and the flaccid quadriplegia are not seen in that condition. If there is any question in an ambiguous case, naloxone can be administered to reverse any opiate intoxication.

Table 4–18 Clinical Findings in 80

Patients With Pontine Hemorrhage

*Number that died in parentheses. Modified from Murata.250

Patient 4–7

A 54-year-old man with poorly treated hypertension was playing tennis when he suddenly collapsed on the court. The blood pressure was 170/ 90 mm Hg; the pulse was 84 per minute; respirations were Cheyne-Stokes in character and 16 per minute. The pupils were pinpoint but reacted equally to light; eyes were slightly dysconjugate with no spontaneous movement, and vestibuloocular responses were absent. The patient was flaccid with symmetric stretch reflexes of normal amplitude and bilateral flexor withdrawal responses in the lower extremities to plantar stimulation. CT scan showed a hemorrhage into the pontine tegmentum. The next morning he was still in deep coma, but now was diffusely flaccid except for flexor responses to noxious stimuli in the legs. He had slow, shallow, eupneic respiration; small, equally reactive pupils; and eyes in the neutral position. Shortly thereafter, breathing became irregular and he died. A 3-cm primary hemorrhage destroying the central pons and its tegmentum was found at autopsy.

The clinical features in Patient 4–7, including coma in the absence of motor responses, corneal reflexes, and oculocephalic responses, predicted the poor outcome.258 In addition, if CT scanning shows a hematoma greater than 4 mL, hemorrhage in a ventral location,259 evidence of extension into the midbrain and thalamus, or hydrocephalus on admission, the prognosis is poor.258

Primary hemorrhage into the medulla is rare.251 Patients present with ataxia, dysphagia, nystagmus, and tongue paralysis. Respiratory and cardiovascular area may occur, leaving the patient paralyzed and unable to breathe, but not unconscious.

Basilar Migraine

Altered states of consciousness are an uncommon but distinct aspect of what Bickerstaff calledbasilar artery migraine,260 associated with prodromal symptoms that suggest brainstem dysfunction. The alteration in consciousness can take any of four major forms: confusional states, brief syncope, stupor, and unarousable coma. Although not technically a destructive

lesion, and with a pathophysiology that is not understood, basilar migraine clearly causes parenchymal dysfunction of the brainstem that is often mistaken for a brainstem ischemic attack.

Alterations in consciousness often last longer than the usual sensorimotor auras seen with migraine. Encephalopathy and coma in migraine occur in patients with familial hemiplegic migraine associated with mutations in a calcium channel261 and in patients with the disorder known as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)262 (see page 276, Chapter 5). The former often have fixed cerebellar signs and the latter multiple hyperintensities of the white matter on MR scanning. Blood flow studies concurrent with migraine aura have demonstrated both diffuse and focal cerebral vasoconstriction, but this is an insufficient explanation for the striking focal symptoms in basilar migraine; however, some clinical lesions suggestive of infarction can be found in patients with migraine significantly more often than in controls.263

Selby and Lance264 observed that among 500 consecutive patients with migraine, 6.8% had prodromal episodes of confusion, automatic behavior, or transient amnesia, while 4.6% actually fainted. The confusional and stuporous attacks can last from minutes to as long as 24 hours or, rarely, more. They range in content from quiet disorientation through agitated delirium to unresponsiveness in which the patient is barely arousable. Transient vertigo, ataxia, diplopia, hemianopsia, hemisensory changes, or hemiparesis changes may immediately precede the mental changes. During attacks, most observers have found few somatic neurologic abnormalities, although occasional patients are reported as having oculomotor palsies, pupillary dilation, or an extensor plantar response. A few patients, at least briefly, have appeared to be in unarousable coma.

Posterior Reversible

Leukoencephalopathy Syndrome

Once believed to be associated only with malignant hypertension (hypertensive encephalopathy),265 posterior reversible leukoencephalopathy syndrome (PRES) is known to be caused by several illnesses that affect endothe-

lial cells, particularly in the posterior cerebral circulation.266 Among the illnesses other than hypertension, pre-eclampsia and immunosuppressive and cytotoxic agents (e.g., cyclosporin, cisplatin) are probably the most common causes. Vasculitis, porphyria, and thrombotic thrombocytopenic purpura are also reported causes, as is occasionally migraine. Posterior leukoencephalopathy is characterized by vasogenic edema of white matter of the posterior circulation, particularly the occipital lobes, but sometimes including the brainstem. Clinically, patients acutely develop headache, confusion, seizures, and cortical blindness; coma is rare. The MRI reveals vasogenic edema primarily affecting the occipital and posterior parietal lobes. Brainstem and cerebellum may also be affected. With appropriate treatment (controlling hypertension or discontinuing drugs), symptoms resolve. In patients with pre-eclampsia

who are pregnant, intravenous infusion of magnesium sulfate followed by delivery of the fetus has a similar effect. If PRES due to preeclampsia occurs in the postpartum period, immediate administration of magnesium sulfate followed by treatment for several weeks with verapamil is often effective, in our experience. The differential diagnosis includes posterior circulation infarction, venous thrombosis, and metabolic coma (Table 4–19 and Patient 5–8).

INFRATENTORIAL INFLAMMATORY DISORDERS

The same infective agents that affect the cerebral hemispheres can also affect the brainstem and cerebellum. Encephalitis, meningitis, and abscess formation may either be part of a more generalized infective process or be

restricted to the brainstem.267 Organisms that have a particular predilection for the brainstem include L. monocytogenes, which often causes brainstem abscesses 268 (Figure 4–13). Occasionally herpes zoster or simplex infection that begins in one of the sensory cranial nerves may cause a segmental brainstem encephalitis.269 Behc¸et’s disease may also cause brainstem inflammatory lesions.270 These disorders usually cause headache with or without nuchal rigidity, fever, and lethargy, but rarely coma. In a minority of instances, the CT scan may show brainstem swelling. The MR scan is usually more sensitive. CSF usually contains an increased number of cells. In bacterial infections cultures are usually positive; in viral infections PCR may establish the diagnosis. Stereotactic drainage of a brain abscess often identifies the organisms; appropriate antimicrobial therapy is usually successful.271

A brainstem disorder often confused with infection is Bickerstaff’s brainstem encephalitis.272 Patients with this disorder have often had a preceding systemic viral infection, then acutely develop ataxia, ophthalmoplegia, longtract signs, and alterations of consciousness including coma. In some patients, MRI reveals brainstem swelling and increased T2 signal273;

in others, the scan is normal. The CSF protein may be elevated, but there are no cells. The disease is believed to be autoimmune in origin related to postinfectious polyneuropathy (the Guillain-Barre´ syndrome) and the related Miller Fisher syndrome.272 The diagnosis can be established by the identification of antiGQ1b ganglioside antibodies in serum.272 Patients recover spontaneously.

INFRATENTORIAL TUMORS

Tumors within the brainstem cause their symptoms by a combination of compression and destruction. Although relatively common in children, primary tumors of the brainstem (brainstem glioma) are rare in adults. Metastatic tumors are more common, but with both primary and metastatic tumors, slowly or subacutely evolving brainstem signs typically establish the diagnosis long before impairment of consciousness occurs. An exception is the rare instance of an acute hemorrhage into the tumor, causing the abrupt onset of paralysis and sometimes coma, in which case the signs and treatment are similar to other brainstem hemorrhages.

CENTRAL PONTINE

MYELINOLYSIS

This is an uncommon disorder in which the myelin sheaths in the central basal pons are destroyed in a single confluent and symmetric lesion. Similar lesions may be found in the corpus callosum or cerebral hemispheres.274 Lesions vary from a few millimeters across to ones that encompass almost the entire base of the pons, sparing only a rim of peripheral myelin. The typical clinical picture is one of quadriparesis, with varying degrees of supranuclear paresis of lower motor cranial nerves and impairment of oculomotor or pupillary responses. A majority of patients become ‘‘locked in.’’ Approximately one-quarter of patients demonstrate impairment of level of consciousness, reflecting extension of the lesion into the more dorsal and rostral regions of the pons.

It is now recognized that most cases of central pontine myelinolysis are due to overly vigorous correction of hyponatremia, giving rise tothe‘‘osmoticdemyelinationsyndrome.’’Since the adoption of current regimens that recommend that hyponatremia be reversed at a rate no greater than 10 mEq/day, the frequency of this once-feared complication has decreased dramatically. On the other hand, a similar syndrome is seen in patients with liver transplantation, possibly due to the use of cyclosporine.274 As liver transplant has become more common, this population is increasing.

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