Twenty-six patients with blunt trauma of the cervical spine, producing a subluxation from a "locked" or "perched" facet, facet destruction with evidence of instability, or a fracture involving the foramen transversarium, underwent preoperative vertebral angiography to determine the incidence of vertebral artery injury. The cervical spine injury in all the patients was deemed unstable and in need of surgical stabilization. Spinal cord injury was present in one-half of the patients studied. Vertebral artery injury was identified angiographically in 12 patients (46%). Occlusion of the vertebral artery near its origin or at the level of the spinal injury was identified in nine patients. An intimal flap, arterial dissection, and a pseudoaneurysm were identified in the remaining three patients. The injury involved the left vertebral artery in all but three patients. In none of the patients did the vertebral artery injury clearly result in neurological dysfunction or other sequelae. After cervical spine fracture or dislocation, vertebral artery injury is more prevalent than commonly believed. The possibility of vertebral artery injury should be considered during the establishment of clinical management schemes for blunt trauma of the cervical spine.

No abstract

Intravenous tissue plasminogen activator is the only therapy approved by the US Food and Drug Administration (FDA) for the treatment of acute ischemic strokes. The National Institutes of Health (NIH)-sponsored study that led to the approval of tissue plasminogen activator to be used in acute ischemic strokes included only individuals 18 years of age and older. We report a case of a pediatric patient who suffered a dominant-hemisphere acute ischemic stroke who was treated with intravenous tissue plasminogen activator. Our patient's symptoms began to resolve 4 hours after treatment, and he had a complete recovery after 8 hours. The clinical outcome was excellent and without complications. Tissue plasminogen activator administration can be safe and effective in younger patients. Randomized, controlled, double-blind studies are needed.

We report a case of migraine-associated ischemic stroke causing amnesia, wherein treatment with propranolol may have been contributory. The possible mechanisms involved in migrainous stroke occurring in association with use of propranolol are discussed.Key words: migrainous stroke, migraine, stroke, thalamic amnesia (Headache 1997;37:594-596) Stroke is a rare but recognized complication of migraine. 1 While propranolol has been incriminated by some to be a potential contributor to this complication, evidence to support that proposal has been scant. We report a case of migrainous stroke wherein treatment with propranolol was associated temporally with stroke onset and may have played a causative role. CASE HISTORYA 47-year-old woman with a long-standing history of episodic headaches characteristic of migraine presented to an emergency department for evaluation and treatment of a particularly severe and protracted migraine attack. In the past, her headaches had occurred either without accompanying aura or with symptomatology characteristic of basilar migraine: bilateral face and hand "numbness and tingling," "slurred" speech, vertigo, gait instability, and horizontal diplopia, all in varying combinations and widely variable in duration. She had been taking 80 mg per day of long-acting (LA) propranolol for migraine prophylaxis and was on estrogen supplementation therapy. She reported a history of hypertension and active cigarette use. Her examination at that time showed right beating nystagmus and gait ataxia. She was treated with intramuscular meperidine and meclizine, but failed to improve. She was instructed to continue taking LA propranolol 80 mg daily.Her headache and associated symptoms worsened over the next 48 hours, and she was admitted to another hospital. Her examination on admission was significant for "gait ataxia on standing position with eyes closed"; she was noted to be fully oriented and cooperative. Due to persistence of headache, LA propranolol was increased to 120 mg per day. Within 24 hours following the increase in her dose of propranolol, she developed acute confusion and agitation and was transferred to the University of South Alabama Medical Center (USAMC).On admission at USAMC, her vital signs included a blood pressure of 155/71, heart rate of 70 beats per minute, respirations of 16 per minute, and she was afebrile. Her neurological examination showed severe stupor without obvious focal findings. Computed tomography (CT) of the brain showed bilateral infarctions of the posterior thalami, left occipital cortex, and left superior cerebellar hemisphere (Figure 1). Brain magnetic resonance imaging (MRI) confirmed these findings. Magnetic resonance angiography (MRA) demonstrated attenuation of flow signal at the level of the distal basilar and left posterior cerebral arteries (Figure 2).Propranolol was discontinued, and she received vigorous volume expansion with intravenous normal saline solution and pharmacologic treatment with oral nimodipine 30 mg every 6 hours, dexamethasone 4 mg IV eve...

A 50-year-old female complained of sudden, severe headache and then collapsed. During EMT transport she suffered a cardiopulmonary arrest but was successfully resuscitated. In the ED, her ECG demonstrated ST segment elevations in multiple leads and her troponin peaked at 7.9.Her neurologic examination was notable for dense stupor, extensor plantar responses bilaterally, and no lateralizing signs. Noncontrasted brain CT (Figure 1) demonstrated blood within the prepontine cistern. A