Treatment of migraine with aura with osteopathic manipulative treatment: a case report with renewed perspectives.

Migraines make up a significant number of office visits every year, yet their pathophysiology and etiology remain largely elusive. This case report presents a 33-year-old patient who originally presented to the emergency department (ED) as a stroke alert and was later determined to have migraine with aura. The patient experienced an acute onset of headache, dizziness, and new-onset expressive aphasia. Before administration of a migraine cocktail, osteopathic manipulative treatment (OMT) was performed and was able to fully resolve all of her symptoms. In an effort to explain the outcomes in this case, a review of the current literature was performed, which provides an interesting perspective on the interplay of the musculoskeletal system and neuroanatomy. The literature establishes that somatic dysfunctions in the cervical vertebrae and trapezius may play a role in migraines and provide rationale for the use of OMT.

A Rare Case of Thiamine Deficiency Leading to Dry Beriberi, Peripheral Neuropathy, and Torsades De Pointes.

Thiamine (vitamin B1) is an essential nutrient and one of the eight B vitamins. As a water-soluble vitamin, thiamine is not stored; therefore, a balanced diet is required to ensure adequate intake of this essential vitamin. Thiamine deficiency is known to cause both wet and dry beriberi, but rarely in combination. Thiamine deficiency has also been known to cause QTc prolongation, but the mechanism remains unclear. In the most severe cases, this can lead to the lethal arrhythmia of torsades de pointes. This case describes a patient who became malnourished after a closed head injury and initially presented with seizure-like activity and syncopal episodes with nonspecific numbness. He was found to have prolonged QTc, leading to torsades de pointes requiring an implanted cardioverter defibrillator. With extensive workup, including genetic testing, the patient was found to have indetectable thiamine levels. With supplementation, the patient no longer had any recorded ventricular arrhythmias, and neurological function improved with only residual tingling in the hands. This case emphasizes the profound effects of thiamine deficiency and why this should be included in our differential diagnosis for patients presenting with the sequelae of the signs and symptoms discussed.

Intracranial Pressure Fluctuations Mimicking Seizures in a Patient With Shunt Malfunction.

SUMMARY: This case describes a patient with new onset of multiple daily paroxysmal stereotyped episodes with alteration of arousal and responsiveness. These episodes pose a diagnostic challenge because they may be misdiagnosed as epileptic seizures because of stereotypy, similarities in semiology, risk factors such as structural abnormality, and rhythmic EEG pattern. A 20-year-old woman with Chiari malformation, spina bifida, and ventriculoperitoneal shunt presented with paroxysmal episodes of change in responsiveness, concerning for seizure activity. Anti-seizure medication was started without amelioration. During the stereotyped episodes, she suffered from paroxysmal headache, drowsiness, poor responsiveness, and relative bradycardia. EEG confirmed relative bradycardia and revealed rapid buildup of generalized rhythmic delta activity without ictal features. Improvement with ICP lowering, and lack of epileptiform activity on EEG or localizing ictal semiology, prompted obtaining shunt imaging and brain MRI. The patient was subsequently diagnosed with shunt malfunction and underwent shunt revision, resulting in complete resolution of her paroxysmal spells. Although common differential diagnosis of brief paroxysmal stereotyped spells includes seizures or psychogenic nonepileptic attacks, this patient's case demonstrates clinical paroxysms caused by intracranial pressure fluctuations (plateau waves). When evaluating patients with possible intracranial pressure abnormality for paroxysmal spells, shunt malfunction should be considered as well.

CO poisoning as an associated risk factor for CVT.

We report a 24year old female who presented with sudden and severe headaches after recent carbon monoxide poisoning. Imaging revealed an acute cerebral venous thrombosis. Prior studies have suggested that carbon monoxide is a risk factor for an acute hypercoagulable state (i.e. DVT). However, little data is available regarding the correlation between carbon monoxide poisoning and cerebral venous thrombosis. This case demonstrates that such a correlation should be considered in acute intracerebral thrombotic events.