Tx and Followup:
This pt is being transitioned from Effexor to Zoloft, his HTN is being addressed with HCTZ, and he will receive rehabilitative treatment from PM&R and physical therapy.
His medical conditions will continue to be followed by psychiatry, medicine, and neurology.
This patient had an atypical presentation for stroke, without any of the classic risk factors. While it is true that headaches are sometimes seen with stroke, this patient had no focal neurologic findings at the time of his presentation, which confused the picture. His headache presentation was most consistent with migraine, if one assumes a primary headache. If one looks further for causes of secondary headache, the differential includes subarachnoid hemorrhage (SAH), aneurysm, acute ischemic cerebrovascular disorder, arteritis, artery dissection, hypertension(HTN), pseudotumor cerebri, infection, and substance use or withdrawal.
In this case, the team did a CT for bleeding including SAH and mass effect, which was negative, blood work to rule out arteritis and infection, and (later) an MRA to examine the arteries, which was also normal everywhere but the L PICA. Physical exam and lumbar puncture ruled out pseudotumor cerebri in this case. That leaves HTN, ischemia/infarct, and substance or drug use or withdrawal.
The patient's systolic blood pressure was elevated on presentation, and with further digging, continued to remain elevated during his hospital course (with diastolic also elevated most of the time). It is possible that his blood pressure had been elevated for quite some time, leading to an occult risk factor. If his headache was a caused by a hypertensive crisis, one would expect his blood pressure to be further elevated on presentation.
The patient was taking Effexor (venlafaxine), which is a Selective Serotonin/ Norepinephrine Reuptake Inhibitor(SNRI), and has both HTN and headaches as possible side effects. Stroke is not listed as a known side effect. However, there is one case study in the literature that describes a patient having a "migraine-like" stroke while having a serotonin syndrome. Serotonin syndrome is caused by too much serotonin in the brain, usually secondary to patients taking SSRIs/ SNRIs and then taking a second serotonin promoter. It does sometimes occur when patients are taking elevated doses of medication. It is unknown how long this patient was taking Effexor before his headaches began or if he experienced any of the other symptoms of serotonin syndrome, including acute mental status changes, involuntary movements, altered muscle tone, and autonomic instability. Even if the patient did not have serotonin syndrome on presentation, it is worth noting that he received sumatriptan while in the hospital, while also receiving his venlafaxine. Could this combination have precipitated a serotonin syndrome? Certainly, however, the patient did not report an increase in symptoms after receiving the drug, so the possibility is very slim.
Cocaine is also associated with stroke in the younger population. It is associated with vasoconstriction, and has been known to cause slow flow in the vertebrobasilar system (which supplies the PICA), among other cerebral infarcts, and HTN. While this patient does not report any cocaine use, it is a possibility to be entertained.
The actual cause of this patientâ€™s infarct may never be known, in part because we do not know when the actual infarct occurred. CT best demonstrates signs of cerebral infarct at least 24 hours after the event. There are cases of CT being used to identify infarcts earlier, but this is generally by identifying secondary signs (like a clot in the MCA) and in the cerebrum rather than the cerebellum. The differential for headaches is very broad, but stroke must be kept in mind especially when no other obvious cause presents itself, as it can often be reversed if found early enough.
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Nanda A, Vannemreddy P, Willis B, Kelley R. Stroke in the young: relationship of active cocaine use with stroke mechanism and outcome. Acta Neurochir Suppl. 2006;96:91-6.
Wardlaw JM, Mielke O. Early signs of brain infarction at CT: observer reliability and outcome after thrombolytic treatment--systematic review. Radiology 2005 May;235(2):444-53. Clinch,CR. Evaluation of Acute Headaches in Adults. Amer Fam Physician. 2001 Feb15;63(4):685-92.
Caplan LR. Posterior Circulation Cerebrovascular Syndromes. www.uptodate.com. Last updated 21Nov2006.
Oliveira-Filho J, Koroshetz WJ. Neuroimaging of acute ischemic stroke. www.uptodate.com. Last updated May 2006.
Pt notes waking up with a mild headache on the day of admission, unrelieved by caffeine consumption, that progressively worsened. The pain was sharp, but throbbing and located behind his left eye and radiating posteriorly. The nausea and vomiting began just after lunch, and shortly after the patient took a motrin for his headache. He denied any fevers, chills, night sweats, recent ill contacts, or diarrhea. The patient was given ativan, morphine, phenergan, zofran and benadryl along with a 1L bolus of NS. CT was performed and determined to be negative for acute pathology. On day 2, the headache had resolved in the AM, but IV phenergan was required for nausea, and the dizziness persisted. The patient reported a headache in the afternoon, unresolved with 2 separate doses of Imitrex (sumatriptan), but partially alleviated with Tylenol. The patient continued to experience pain the following day, so a repeat CT was done, which showed a â€śprobable left cerebellar infarctâ€ť.
PMHx: Hypertriglyceridemia, psoriasis, anxiety, G6PD, Crohns
Meds: Lopid (gemfibrozil), Effexor (venlafaxine)
Allergies: Iodine, Primaquin