Objective To review characteristics and outcomes of all cases of visual snow seen at our institution, with attention to possible triggering events or comorbidities. Methods This is a retrospective case series of patients seen at our tertiary care center from January 1994 to January 2020. Charts were reviewed if they contained the term “visual snow”. Results Of the 449 charts reviewed, 248 patients described seeing visual snow in part or all of their vision. Thirty-eight reported transient visual snow as their typical migraine aura. Of the remaining 210 patients, 89 were reported to have either an inciting event or contributing comorbidity for their visual snow symptoms, including: Post-concussion (n = 15), dramatic change in migraine or aura (n = 14), post-infection (n = 13), hallucinogen persisting perception disorder (n = 10), ocular abnormalities (n = 7), idiopathic intracranial hypertension (n = 4), neoplastic (n = 1), and posterior cortical atrophy (n = 1). Some patients had partial improvement with benzodiazepines (n = 6), lamotrigine (n = 5), topiramate (n = 3) and acetazolamide (n = 3). Presenting characteristics were similar, but patients with visual snow attributed to an inciting event or contributing comorbidity were more likely to have some improvement in their symptoms by last follow-up compared to spontaneous visual snow ( p < .001). Conclusions Though most cases of visual snow are spontaneous, potential secondary causes should be recognized by clinicians. Patients who develop visual snow after an inciting event or related to an underlying comorbidity may have a better prognosis than those in whom it develops spontaneously. In select cases, treatment of the suspected underlying cause may significantly alleviate the otherwise typical intractable visual disturbances associated with visual snow.
The SPG is known to play an integral role in the pathophysiology of facial pain and the trigeminal autonomic cephalalgias, although its exact role in the generation and maintenance of migraine headache remains unclear. Regional anesthetic suprazygomatic SPG block is potentially effective for immediate relief of SM. We believe the procedure is simple to perform and has minimal risk.
Central alveolar hypoventilation disorders denote conditions resulting from underlying neurologic disorders affecting the sensors, the central controller, or the integration of those signals leading to insufficient ventilation and reduction in partial pressures of oxygen. We report a patient who presented with a left lateral medullary ischemic stroke after aneurysm repair who subsequently developed a rare complication of CAH. Increased awareness of this condition's clinical manifestations is crucial to make an accurate diagnosis and understand its complications and prognosis.
Left ventricular noncompaction (LVNC) is a rare cause of cardiomyopathy that can lead to systemic embolism and ischemic stroke. LVNC results from the arrest of ventricular myocardium compaction during embryogenesis. Multiple other cardiac complications coexist with this cardiomyopathy, and one of the potential consequences is cardioembolic events causing ischemic stroke. This condition can be underdiagnosed or misdiagnosed as hypertrophic or dilated cardiomyopathy. We report a patient who presented with recurrent embolic ischemic stroke secondary to LVNC that was overlooked on initial transthoracic echocardiographic studies. After an unremarkable laboratory workup, transesophageal echocardiogram (TEE) revealed noncompaction of the myocardium within the apex of the left ventricle, confirmed by cardiac magnetic resonance imaging (MRI). The patient was anticoagulated with warfarin and discharged to a rehabilitation facility. Increased understanding and awareness of the diagnosis, clinical manifestations, and management of LVNC are advised, particularly in patients with recurrent embolic stroke of undetermined source. Screening of all first-degree relatives with this familial condition is recommended as well, as appropriate treatment can prevent cardiac complications and sudden death.
Introduction:
Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal intracranial arterial constriction and dilation that occurs spontaneously or as a result of a stimulant. The authors present a case of RCVS in a patient who presented with a new-onset thunderclap headache a day after carotid endarterectomy (CEA). RCVS has been rarely reported after CEA.
Case Report:
A 65-year-old woman was evaluated for a new-onset thunderclap headache a day after left-sided CEA. Computed tomography (CT) of the head revealed left frontal and parietal subarachnoid hemorrhage (SAH). CT angiography did not show any saccular aneurysms or vessel stenosis. The initial impression was SAH related to reperfusion injury after carotid revascularization. Seven days postoperatively, the patient returned to the hospital with a persistent headache. CT revealed SAH in the vertex of the frontal region bilaterally. Magnetic resonance angiogram (MRA) of the head revealed multifocal stenosis of the intracranial circulation bilaterally. A follow-up MRA 9 weeks postoperatively showed interval improvement of the caliber of the circle of Willis branches and significant improvement of the multifocal stenosis. The patient was diagnosed with RCVS as a result of CEA.
Conclusion:
The authors advise clinicians to consider RCVS as a cause of thunderclap headache or recurrence of a severe headache shortly after CEA—particularly with the presence of a nonaneurysmal convexity SAH.
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