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The Case
The patient is a 50-year-old woman with a witnessed sudden onset of severe
pancranial headache, nausea and vomiting that progressed to a decreased level
of consciousness. She was brought to the emergency room by ambulance within
an hour of ictus. Clinical examination demonstrated a Glascow coma score
of 11 (Best Eye, 3; Verbal, 3; Motor 5), with symmetric and reactive pupils
and a subtle right hemipariesis. Bloodwork, including coagulation studies,
was normal. The CT showed subarachnoid blood centered in the perimesencephalic
cistern, but extending into the Sylvian fissures and ambient cisterns bilaterally
(see figure). Enlargement of the lateral, third, and fourth ventricles suggested
an acute communicating hydrocephalus. This was treated by placement of an
external ventricular drain, after which her clinical condition stabilized
with a normal level of consciousness and no focal deficits. CT angiography
and a subsequent catheter angiogram demonstrated no obvious vessel abnormalities.
Take the Gray Matters Survey
Please indicate how you would proceed for this patient by answering the brief
multiple choice survey questions at www.aansneurosurgeon.org (select the
Gray Matters Surveys link in the tool bar and take the survey); an optional
comment field is provided at the survey’s end.
• Web Address: www.aansneurosurgeon.org
• Take the Survey: Idiopathic or Aneurysmal Subarachnoid Hemorrhage
A synopsis of all responses will be published in the next issue; signed responses
will be considered for publication.
Considerations
Despite similar early clinical and radiographic appearances, the incidence,
etiology, and natural history of perimesencephalic subarachnoid hemorrhage
is significantly different from that of aneurysmal rupture. Perimesencephalic
hemorrhage occurs with an annual incidence of 0.5 cases per 100,000 people
and is responsible for 15 percent of all spontaneous subarachnoid hemorrhages
(2). Its etiology is still uncertain, but current theories include both arterial
and venous causes (6). Outcome after perimesencephalic hemorrhage is clearly
better than after aneurysmal hemorrhage, with long-term follow-up studies
demonstrating equal life expectancy and no higher risk of rebleeding compared
with the general population (2, 3).
Differentiating perimesencephalic etiology from other causes of subarachnoid hemorrhage in the acute stage, however, remains a difficult problem, and there is no consensus on the management of spontaneous subarachnoid hemorrhage with a normal initial angiogram. Repeat angiography finds roughly 18 percent of occurrences in those whose initial cerebral angiogram was negative, with the vast majority of initial false negatives occurring with a nonperimesencephalic hemorrhage pattern. In patients with a typical perimesencephalic pattern, however, the false negative rate of initial angiography is less than 1.5 percent (4, 5, 8). MRI of the brain and spinal cord have revealed nonaneurysmal causes (pituitary adenoma, spinal arteriovenous malformation) in 4 percent of angiogram-negative SAH cases, but none of these occurred in cases with a typical appearance on CT of perimesencephalic hemorrhage (7).
Ruptured posterior circulation aneurysms can present with a radiographic pattern of perimesencephalic hemorrhage in more than 15 percent of cases. Conversely, there is a 5 percent to 10 percent likelihood of finding a posterior circulation aneurysm in any patient with a perimesencephalic hemorrhage pattern (1). The specific hemorrhage pattern and its differential diagnosis, therefore, should guide decision-making in these cases.
Alim P. Mitha, MD, MS, is chief resident, and Rajiv Midha, MD, MSc, is professor and deputy head of the Department of Clinical Neurosciences and chief of the Division of Neurosurgery at the University of Calgary in Canada. The authors reported no conflicts for disclosure.
References
- Alen JF, Lagares A, Lobato RD, Gomez PA, Rivas JJ, Ramos A: Comparison between perimesencephalic nonaneurysmal subarachnoid hemorrhage and subarachnoid hemorrhage caused by posterior circulation aneurysms. J Neurosurg 98:529–535, 2003
- Flaherty ML, Haverbusch M, Kissela B, Kleindorfer D, Schneider A, Sekar P, et al.: Perimesencephalic subarachnoid hemorrhage: incidence, risk factors, and outcome. J Stroke Cerebrovasc Dis 14:267-271, 2005
- Greebe P, Rinkel GJ: Life expectancy after perimesencephalic subarachnoid hemorrhage. Stroke 38:1222-1224, 2007
- Huttner HB, Hartmann M, Köhrmann M, Neher M, Stippich C, Hahnel S, et al.: Repeated digital substraction angiography after perimesencephalic subarachnoid hemorrhage? J Neuroradiol 33:87-89, 2006
- Jung JY, Kim YB, Lee JW, Huh SK, Lee KC: Spontaneous subarachnoid haemorrhage with negative initial angiography: a review of 143 cases. J Clin Neurosci. 13:1011-1017, 2006
- Matsumaru Y, Yanaka K, Matsumura A: Is perimesencephalic nonaneurysmal hemorrhage of venous origin? Stroke 35:2753-2754, 2004
- Rogg JM, Smeaton S, Doberstein C, Goldstein JH, Tung GA, Haas RA: Assessment of the value of MR imaging for examining patients with angiographically negative subarachnoid hemorrhage. AJR Am J Roentgenol 172:201-206, 1999
- Topcuoglu MA, Ogilvy CS, Carter BS, Buonanno FS, Koroshetz WJ, Singhal AB: Subarachnoid hemorrhage without evident cause on initial angiography studies: diagnostic yield of subsequent angiography and other neuroimaging tests. J Neurosurg 98:1235-1240, 2003
| Responses: Minimally Symptomatic Cervical Spondylotic Myelopathy
AANS Neurosurgeon 17(1):47-48, 2008 THE CASE: Conservative Management or Surgery for a Patient With Minimally Symptomatic Cervical Spondylotic Myelopathy? Survey Results Summary Of those advocating surgery, slightly more than half would recommend a posterior approach. Specific comments related to the posterior approach included recommending laminectomy alone, laminoplasty over three levels, and laminectomy with fusion. A minority opinion was for both an anterior and posterior decompressive procedure, with one suggestion specifically of disc removal and interbody fusion augmented with plating at C4-C5 and C5-C6 as well as a C3-C6 laminectomy. Case Commentary Late stage cervical myelopathy rarely improves with treatment. Early stage
treatment, such as in the patient presented here, often reverses symptoms and
prevents progression. I prefer simple decompression unless a fusion is clearly
indicated, but I X-ray yearly and fuse in the few cases that develop deformity
with time. This patient has obvious myelopathy by clinical and radiographic criteria
and has suffered from “worsening” neck pain for two years. It is inappropriate
to consider him minimally symptomatic. Furthermore, the term minimally myelopathic
represents a contradiction in terms, as any myelopthy is significant. He should
be offered surgical treatment before his myelopathy progresses, as it is likely
to do within his lifetime. Furthermore, this is precisely the type of patient
who is at risk for central cord injury with mild trauma. An anterior cervical
decompression and fusion would serve to treat his myelopathy, protect him against
future cord injury and address his two-year history of neck pain. |
