Transient contrast encephalopathy after carotid artery stenting.

PURPOSE: To report an unusual case of transient contrast encephalopathy arising after carotid artery stenting. CASE REPORT: An 82-year-old right-handed man with a recent history of transient ischemic events was admitted to the hospital for evaluation of carotid artery disease. During cerebral angiography, which identified a 90% right internal carotid artery stenosis, the patient received 25 mL of an ionic, low-osmolar contrast agent (ioxaglate) in each carotid artery. The following day he underwent successful carotid stenting, during which 180 mL of ioxaglate were used. He developed rapidly worsening confusion and left hemiparesis on the table. Noncontrast computed tomography showed marked cortical enhancement and edema of the right cerebral hemisphere in the distribution of the right anterior and middle cerebral arteries. The patient improved rapidly and by day 2 was completely recovered; magnetic resonance imaging documented no cortical edema and normal sulci. One month after the procedure, he was well, with patent carotid arteries. CONCLUSIONS: Transient neurotoxicity after carotid interventions must be differentiated from massive cerebral infarction and hyperperfusion syndrome, but the prognosis is excellent. However, subsequent contrast studies in a patient with this complication should be undertaken with extreme caution.

Carotid artery stenting in patients with high-risk anatomy for carotid endarterectomy.

PURPOSE: To report the results of carotid artery stenting (CAS) in patients considered to have high-risk anatomical characteristics for carotid endarterectomy. METHODS: CAS was performed in 39 carotid arteries of 37 consecutive patients (26 men; mean age 72 +/- 8 years, range 56-88) who met the criteria for high-risk surgical anatomy: previous ipsilateral carotid endarterectomy (20/39, 51.3%), common carotid bifurcation above the mandibular angle (5/39, 12.8%), contralateral carotid artery occlusion (15/39, 38.5%), or previous radiation therapy to the neck (1/39, 2.6%). Palmaz, Integra, or Wallstents were deployed via a percutaneous femoral artery access. Independent neurological evaluation was performed at specified time points, and a dedicated committee adjudicated all clinical events. RESULTS: Procedural success was 100%, with no major in-hospital complications. Neurological events were rare. Only 1 (2.6%) transient ischemic attack occurred prior to discharge; at 30 days, 1 (2.6%) additional minor stroke had been observed, giving a 2.6% cumulative 30-day "death plus any stroke" rate. Over a mean 11 +/- 6-month follow-up, 2 (5.4%) patients died of nonneurological causes, but there were no strokes. CONCLUSIONS: CAS is a viable endovascular revascularization technique that can be performed safely and effectively in patients with high-risk anatomy for carotid endarterectomy.

Postprocedural hypotension after carotid artery stent placement: predictors and short- and long-term clinical outcomes.

PURPOSE: To describe the predictors of persistent hypotension after carotid artery stent (CAS) placement and define the clinical outcome of patients with this hemodynamic disturbance. MATERIALS AND METHODS: One hundred forty CAS procedures were performed in 133 consecutive patients. Post-CAS hypotension-defined as a greater than 40 mm Hg decrease in arterial pressure without evidence of hypovolemia, with a systolic pressure lower than 90 mm Hg at the end of CAS and lasting at least 1 hour-was observed in 25 patients (group 1); 108 patients did not have hypotension (group 2). RESULTS: Post-CAS hypotension developed in 33.9% of cases after balloon-expandable stent placement versus in 13.6% of cases after self-expanding stent placement (P =.04). In-hospital minor ipsilateral strokes occurred in 16% of cases in group 1 versus in 3% of cases in group 2 (P =.03). There was one (0.9%) major stroke (transient) and three (2.6%) transient ischemic attacks, all of which occurred in group 2 (not significant vs group 1 for both conditions). At 10 months +/- 4 (SD) of follow-up, there was greater total mortality in group 1 than in group 2 (20% vs 4%, P =.02), whereas neurologic events did not differ significantly between the groups. CONCLUSION: Hypotension due to carotid sinus stimulation is frequent after CAS with balloon-expandable stents. This phenomenon correlates with increased in-hospital complications and long-term risk of death.

MRI in vitamin B12 deficiency myelopathy.

BACKGROUND: Little is known about vitamin B12 deficiency myelopathy's magnetic resonance imaging (MRI) manifestations and their relationship to the onset, evolution, and resolution of neurologic signs and symptoms. METHODS: We present a case and review eleven additional reported cases of subacute combined degeneration of the spinal cord detected by MRI. RESULTS: Our patient had increased T2-weighted signal and gadolinium contrast enhancement of the posterior columns in the cervical and thoracic regions and enhancement of the lateral columns in the high cervical region. This is a case with imaging evidence for lateral column lesions. Two prior reports have shown posterior column enhancement. T1-weighted images may show decreased signal in the posterior columns and sometimes demonstrate reversible spinal cord swelling. MRI abnormalities typically improve after vitamin replacement therapy. However, clinical signs may persist despite resolution of imaging abnormalities, and these abnormalities do not always resolve completely. In addition, symptoms may precede the imaging abnormality. CONCLUSIONS: Vitamin B12 deficiency may produce an increased T2-weighted signal, decreased T1-weighted signal, and contrast enhancement of the posterior and lateral columns of the spinal cord, mainly of the cervical and upper thoracic segments. Because the symptoms may precede any imaging abnormality, it is clear that spinal cord MRI may not be a highly sensitive, early test for subacute combined degeneration.

Hydrocephalus: obliterated perimesencephalic cisterns and the danger of sudden death.

OBJECTIVE: We reported a possible risk factor which could identify patients with chronic hydrocephalus who are risk for sudden death. METHODS: A retrospective review of medical records and computed tomographic (CT) scans was conducted on three patients with chronic hydrocephalus who suffered acute cardiorespiratory arrest without those signs which are normally associated with a progressive worsening of hydrocephalus. RESULTS: All three of these patients were awake and communicative shortly before the life threatening or terminal event. All had experienced some recent worsening of neurologic signs or symptoms, but none had shown a progressive impairment of consciousness or major neurologic decline ordinarily associated with life threatening elevation of intracranial pressure. Absence of the perimesencephalic cisterns on head CT scans done prior to or just after the life threatening event was the only new radiologic finding common to all these patients. CONCLUSIONS: The absence of the perimesencephalic cisterns in an awake and alert patient with severe hydrocephalus indicates that the patient may be at risk for neurogenic cardiorespiratory failure. In such cases, (especially when there has been a recent, albeit mild, change in neurologic signs or symptoms), the neurologist should urge emergency ventriculostomy or shunting for the hydrocephalus.

Myelinolysis after correction of hyponatremia.

Myelinolysis is a neurologic disorder that can occur after rapid correction of hyponatremia. Initially named "central pontine myelinolysis," this disease is now known to also affect extrapontine brain areas. Manifestations of myelinolysis usually evolve several days after correction of hyponatremia. Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobulbar palsy, and mental disorders ranging from mild confusion to coma. Death may occur. The motor and localizing signs of myelinolysis differ from the generalized encephalopathy that is caused by untreated hyponatremia. Experiments have duplicated the clinical and pathologic features of myelinolysis by rapidly reversing hyponatremia in animals. Myelinolysis is more likely to occur after the treatment of chronic rather than acute hyponatremia and is more likely to occur with a rapid rate of correction. The exact pathogenesis of myelinolysis has not been determined. Optimal management of hyponatremic patients involves weighing the risk for illness and death from untreated hyponatremia against the risk for myelinolysis due to correction of hyponatremia. Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a rate less than 10 mmol/L in any 24-hour period.

Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia.

Neurologic disorders developing after correction of severe, symptomatic hyponatremia were studied in 14 patients. None had a hypoxic event or other identifiable cause for the neurologic illness. Neurologic deterioration began about 3 days after correction and often followed a period of improvement in hyponatremic encephalopathy. Although the symptoms were as mild as transient confusion in 1 patient, they were more severe in the others. Typically, spastic quadriparesis, pseudobulbar palsy, and impairment in the level of consciousness progressed for up to 7 days. Improvement generally began 2 weeks after correction and continued for up to a year in some patients. Routine spinal fluid analysis was usually normal, but myelin basic protein concentration was elevated in all patients in whom it was measured. Electroencephalograms commonly showed nonfocal slowing. Brainstem auditory evoked potential latencies were prolonged in some patients. Brain imaging was normal in the initial week of illness, while later scans, obtained in 9 patients, showed central pontine and/or symmetric extrapontine lesions. The clinical manifestations and distribution of lesions seen on imaging demonstrate that neurologic illness following correction of hyponatremia is due to myelinolysis. Although this neurologic disorder typically followed an elevation in serum sodium > 18 mEq/L/24 hr, it sometimes followed a rise as slow as 10 mEq/L/24 hr and 21 mEq/L/48 hr. Whenever possible, the rate of correction of hyponatremia should be kept below these values in order to minimize the risk of myelinolysis.

Deafness after bilateral midbrain contusion: a correlation of magnetic resonance imaging with auditory brain stem evoked responses.

A 46-year-old woman became deaf after a closed head injury. When a computed tomographic scan failed to disclose the cause, conversion disorder was suspected. Magnetic resonance imaging, however, showed bilateral contusions of the inferior colliculi, providing objective evidence for an organic cause of hearing loss. Auditory brain stem evoked responses and stapedial reflexes also provided objective evidence of brain stem injury. This case illustrates the phenomenon of dorsal midbrain injury after head trauma. It indicates the sensitivity of magnetic resonance imaging for small focal lesions after head trauma, and it demonstrates some difficulties in the diagnosis of "hysterical" deafness.

Pontine myelinolysis after correction of hyponatremia during burn resuscitation.

Central pontine myelinolysis is a neurologic disease produced by the rapid correction of hyponatremia. This report describes the occurrence of central pontine myelinolysis in a patient with burns. The natural history of this paralyzing condition and suggestions for its prevention are discussed. Severely burned and hyponatremic patients are at risk for this disorder because a large amount of sodium ion is typically required for the treatment of burn shock. Awareness of this phenomenon and avoidance of rapid correction of hyponatremia are essential to its prevention.

Handcuff neuropathies.

Compressive neuropathy due to tight application of handcuffs occurred in 5 patients. The superficial radial nerve was affected in 8 hands and the median nerve in two. Neurologic deficits persisted as long as 3 years after handcuffing. Nerve conduction studies helped to exclude malingering and other diagnoses. All patients had been intoxicated when handcuffed or had been arrested with force. The handcuff mechanism, which allows accidental overtightening after application, is an unrecognized factor in these neuropathies.

Acute blood pressure elevation can mimic arteriographic appearance of cerebral vasculitis--(a postpartum case with relative hypertension).

A 35-year-old woman presented 9 days postpartum with severe headache, arterial hypertension, and left parietal symptoms. A cerebral angiogram revealed widespread irregular areas of narrowing and dilatation, highly suggestive of vasculitis. The hypertension was treated successfully. A repeat angiogram 9 days later was almost completely normal. As this course is inconsistent with isolated cerebral vasculitis, and because the angiogram normalized with antihypertensive therapy, it is likely that the angiographic findings were secondary to hypertension. Experimental data in fact show that acute hypertension can produce areas of cerebrovascular spasm and dilatation. Recognition that angiographic findings suggestive of cerebral vasculitis are nonspecific and may be due to hypertension should prevent unnecessary treatment for vasculitis in such patients.

Toxoplasmic myelitis mimicking intramedullary spinal cord tumor.

Toxoplasma gondii causes cerebral infection in individuals with impaired immunologic defense mechanisms. We report a case of toxoplasmic myelitis. Spinal cord toxoplasmosis has not been previously documented except in congenital infection.