A Young Man With a Thunderclap Headache and Sudden Loss of Consciousness

Author:
Ronald N. Rubin, MD—Series Editor

Citation:
Rubin RN. A young man with a thunderclap headache and sudden loss of consciousness. Consultant. 2018;58(1):38-39.

A 22-year-old college student collapsed while crossing the campus midday on his way to classes. He remained down until emergency personnel arrived on the scene. Onlookers noted that he had held his head just before collapsing. He awakened somewhat in the ambulance but remained obviously obtunded and somnolent, with impaired mentation. He was able to minimally answer questions and, as such, informed the emergency department (ED) staff about a sudden and violent headache immediately preceding the collapse. He denied having taken any medications or illicit drugs.

His vital signs included a blood pressure of 125/92 mm Hg and a pulse rate of 76 beats/min. He was afebrile. His pupils were round, equal, and reactive. He was somnolent but arousable and quite disoriented, but there were no focal neurologic deficits. The rest of the examination findings were essentially normal, and he appeared to be an otherwise healthy young man.

Which one of the following is an incorrect statement regarding the diagnostic and/or therapeutic strategies for this patient?

1. Computed tomography (CT) scanning within 3 days of symptom onset is virtually 100% sensitive for detecting subarachnoid hemorrhage (SAH), whereas digital subtraction angiography (DSA) is the standard of care to diagnose and define aneurysm as the cause.
2. Lumbar puncture (LP) to assess for xanthochromia is an excellent tool to detect SAH when initial CT scans of the head are negative.
3. Of the associated medical maneuvers used in the peri-rupture period, calcium-channel blockade with nimodipine to reduce or prevent delayed cerebral ischemia (DCI) is most efficacious.
4. While surgical clipping and endovascular aneurysm obliteration are both effective techniques in eliminating the immediate risk of rerupture, surgical clipping may be advantageous in the case of the patient described here.

Answer and discussion on next page.

Answer: B is the incorrect statement

The case presented here is the classic and dramatic “thunderclap headache,” “worst headache of one’s life” presentation of SAH. This syndrome has certain well-known and data-supported sets of epidemiologic and demographic characteristics that frame the situation. For example, SAH causes between 5% and 10% of strokes in the United States¹; such patients typically are younger than those who sustain strokes associated with hypertension and other etiologies.

Intracranial aneurysm rupture is the cause of 80% of cases of SAH occurring in the absence of trauma.¹ Such aneurysms are not uncommon in the general population, and they most often occur at branch points of the cerebral circulation—a very frequent location is the branch point between the anterior cerebral artery and the middle cerebral artery along the circle of Willis. When such an aneurysm ruptures, a true intracranial catastrophe ensues, with a mortality rate of 25% to 50% in the acute setting.^1-3 In addition, acute SAH is one of the causes of acute and unexpected sudden death in which a person does not survive long enough to obtain medical attention.^1-3

The clinical presentation of SAH includes a sudden and severe headache promptly followed by nausea, emesis, photophobia, and a variety of neurologic deficits, depending on the location of the bleed. Most patients will manifest some degree of altered mentation along the way, ranging from mild confusion and lethargy to dense coma.^2,3 The more profound the diminished mentation, the worse the prognosis.^2,3

A disturbing additional point is that as many as half of patients who develop SAH have experienced a lesser event from a lesser bleed in the prior 2 months; the prognosis of patients in this subgroup is even worse.^2,3 Hopefully, future studies will lead to techniques that can more efficiently and accurately detect such sentinel bleeds so as to prevent a catastrophic SAH event.

The mortality of SAH is a result of rerupture and/or the development of cerebral vasospasm and DCI in the weeks after the event. Additional morbidity and neurologic disability, such as the development of hydrocephalus, accrue from the effects of bleeding within the brain. Preventing rerupture is possible by a variety of surgical techniques. Prevention of vasospasm, however, remains problematic, although a number of data-derived adjuvant medical treatments are the current standard of care.

Of course, the initial part of any management approach is prompt and accurate diagnosis. Currently, this means immediate noncontrast CT imaging of the head, which is essentially 100% sensitive in the initial 3 days for the presence of subarachnoid bleeding.^2,4,5 Additionally and importantly, CT has the ability to detect an intraparenchymal hematoma and/or enlarged ventricular horns pathognomonic of hydrocephalus, thus quickly demonstrating the need for immediate surgical intervention.^2,4,5 We therefore can quickly dismiss Answer B, the use of LP to demonstrate either gross blood or xanthochromia in the cerebrospinal fluid as evidence of SAH, especially after negative CT findings in the acute setting. The challenge of differentiating a traumatic LP from a bona fide SAH dates back to this author’s residency, and better, safer, and more accurate diagnostic methods are available for SAH such that Answer B is a weak statement at best and is not the best choice among the strategies offered above. DSA is the current standard for defining the presence of and the precise anatomy of an aneurysm, thus establishing the diagnosis as well as indicating the optimal means of surgical management.⁴ Thus, Answer A is a strong and accurate statement.

A variety of medical maneuvers are used adjunctively to prevent or at least lessen the DCI and/or vasospasm events that occur in up to 70% of SAH cases.^2,5 The current standard of care is the use of the vasodilator and calcium-channel blocker nimodipine, which has been shown to lessen the incidence of vasospasm and improve clinical outcomes when routinely administered to all SAH patients for a 21-day period after the event.^2,5 Thus, Answer C is a correct statement.

Finally, essentially all patients with SAH require a surgical procedure to address the pathologic anatomy of the aneurysm so as to prevent deadly rerupture. Two excellent methods are currently available: open surgical clipping and endovascular obliteration. The former is the traditional open craniotomy procedure in which the subarachnoid space is opened, the aneurysm is exposed, and a clip is placed across the aneurysm to prevent blood flow into it. Advantages of this approach include a lower rerupture rate and better results for SAH cases complicated by hydrocephalus or intraparenchymal hematoma.⁵ The rapidly developing endovascular techniques involve advancing a catheter into the cerebral circulation to the aneurysm site, and then using coils to achieve thrombosis and ablate the aneurysm.⁵ Advantages of endovascular embolization include its markedly less-invasive nature, lower short-term (1-year) mortality rates, better functional outcomes, and lower post-event seizure incidence.^6,7 A disadvantage is the higher rate of rerupture, such that this procedure is usually offered to patients older than 40.² Answer D summarizes the current surgical approaches to SAH and is indeed, for now, a correct statement.

Patient Follow-Up

In the ED, noncontrast CT of the head revealed the presence of an acute SAH and enlarged temporal horns. DSA was then performed and revealed the presence of an aneurysm of the bifurcation of the middle cerebral and anterior cerebral arteries. In light of the patient’s young age, the location of the aneurysm, and the presence of hydrocephalus, open surgical clipping was chosen for repair. The procedure revealed a lobulated aneurysm that was successfully clipped. The patient had an uneventful perioperative period (and received nimodipine), during which there was progressive improvement in mentation and hydrocephalus, obviating the need for a shunting procedure. 

Ronald N. Rubin, MD, is a professor of medicine at the Lewis Katz School of Medicine at Temple University and is chief of clinical hematology in the Department of Medicine at Temple University Hospital in Philadelphia, Pennsylvania.

References:

1. Rincon F, Rossenwasser RH, Dumont A. The epidemiology of admissions of nontraumatic subarachnoid hemorrhage in the United States. Neurosurgery. 2013;73(2):217-222.
2. Lawson MT, Vates GE. Subarachnoid hemorrhage. N Engl J Med. 2017;​377(3):257-266.
3. Kowalski RG, Claassen J, Kreiter KT, et al. Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA. 2004;291(7):866-869.
4. Meurer WJ, Walsh B, Vilke GM, Coyne CJ. Clinical guidelines for the emergency department evaluation of subarachnoid hemorrhage. J Emerg Med. 2016;50(4):696-701.
5. Connolly ES Jr, Rabinstein AA, Carhuaspoma JR, et al; American Heart Association Stroke Council, Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Council on Cardiovascular Surgery and Anesthesia; and Council on Clinical Cardiology. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711-1737.
6. Spetzler RF, McDougall CG, Zabramski JM, et al. The Barrow Ruptured Aneurysm Trial: 6-year results. J Neurosurg. 2015;123(3):609-617.
7. Molyneux AJ, Birks J, Clarke A, Sneade M, Kerr RSC. The durability of endovascular coiling versus neurosurgical clipping of ruptured cerebral aneurysms: 18 year follow-up of the UK cohort of the International Subarachnoid Aneurysm Trial (ISAT). Lancet. 2015;385(9969):691-697.