Spinal Spinal Subarachnoid Hemorrhage Research Articles

Assessment relationship between the femoral artery vasospasm and dorsal root ganglion cell degeneration in spinal subarachnoid hemorrhage: an experimental study.

Animal proof of principle study. To investigate neurodegeneration in rabbit L4-dorsal root ganglion (DRG) cells by creating experimental spinal subarachnoid hemorrhage (SAH), we aimed to show the neuronal pathway between L4-DRG and femoral artery. Ataturk University, Medical Faculty, Animal Laboratory, Erzurum, Turkey. This study was designed on 20 rabbits, which were randomly divided into three groups: Spinal SAH (n = 8), SHAM (n = 6), and control (n = 6) groups. Animals were followed for 20 days and then killed. Vasospasm index values of the femoral artery and neuron density of L4-DRG were analyzed. The number of degenerated neurons in DRG was higher in the spinal SAH than the control and SHAM groups (p < 0.001). But, the difference between the control group and the SHAM group was not significant. Normal neuron densities were significantly lower in the spine SAH group compared to the SHAM and the control groups. There was a statistically significant increase in vasospasm index values of the spinal SAH group compared to the other two groups (p < 0.001). Decreased volume of the femoral artery lumen was showed in animals with spinal SAH compared with control and SHAM groups. Increased degeneration of the L4 dorsal root ganglion in animals with spinal SAH was also demonstrated. Our findings might shed light on the planning of future experimental studies and evaluating the clinical relevance of such studies.

Important interaction between urethral taste bud-like structures and Onuf's nucleus following spinal subarachnoid hemorrhage: A hypothesis for the mechanism of dysorgasmia

BackgroundWe previously postulated that orgasmic sensation may occur through recently discovered genital taste bud-like structures. The interaction between the pudendal nerve and Onuf's nucleus may be important for developing orgasmic information. The study aims to investigate whether ischemic damage to Onuf's nucleus-pudendal network following spinal subarachnoid hemorrhage (SAH) causes taste bud degeneration or not. MethodsThe study was conducted on 22 fertile male rabbits who were divided into three groups: control (GI; n=5), SHAM (GII; n=5) and study (GIII; n=12). Isotonic solution, .7cm3, for the SHAM, and .7cm3 homologous blood was injected into spinal subarachnoid spaces at S2 level of the study group. Two weeks later, Onuf's nucleus, pudendal ganglia and the taste bud-like structures of the penile urethra were examined histopathologically. Degenerated neuron densities of Onuf's nucleus, pudendal ganglia and atrophic taste bud-like structures were estimated per mm3 and the results analyzed statistically. ResultsThe mean degenerated neuron densities of taste bud-like structures, Onuf's nucleus and pudendal ganglia were estimated as 2±1/mm3, 5±1/mm3, 6±2/mm3 in GI; 12±4/mm3, 35±9/mm3, 188±31/mm3, in GII and 41±8/mm3, 215±37/mm3, 1321±78/mm3, in GIII. Spinal SAH induced neurodegeneration in Onuf's nucleus, pudendal ganglia and taste bud atrophy was significantly different between GI/GII (p<.005); GII/GIII (p<.0005) and GI/GIII (p<.0001). ConclusionIschemic neuronal degenerations of Onuf's nucleus and pudendal ganglia following spinal SAH lead to genital taste bud-like structure atrophy. This mechanism may be responsible for sexual anhedonia and sterility in cases with spinal cord injury, which has not been documented so far. More studies are needed.

Ruptured Spinal Aneurysms: Diagnosis and Management Paradigms

Spinal aneurysms (SA) are rare neurovascular pathologies with an unclear natural history and management strategy. We review the clinical and radiologic manifestations, management, and outcome of patients who presented with spinal subarachnoid hemorrhage (SAH) secondary to ruptured spinal aneurysms over a 10-year period. We provide a literature review about this condition and its management. All patients diagnosed with nontraumatic spinal SAH were collected from a single-center prospectively maintained database of patients with SAH between January 2010 and January 2020. Patients diagnosed with spinal aneurysms were reviewed. For each patient, demographic data, clinical presentation, imaging findings, management strategies, and outcomes are reviewed and discussed. Between January 2010 and January 2020, ten patients were diagnosed with nontraumatic spinal SAH (3 patients presented with isolated spinal SAH and 7 patients with concomitant spinal and posterior fossa SAH). Among those, 4 patients were found to have a spinal aneurysm as the cause of SAH. The aneurysms were located in the cervical regions in 3 patients (75%) and at the thoracic level in 1 patient. Two aneurysms (50%) involved the anterior spinal artery, and 2 aneurysms (50%) involved a radiculomedullary artery. One aneurysm was a flow-related aneurysm of the anterior spinal artery in the setting of bilateral vertebral artery occlusion and was treated by surgical clipping with good outcome. Three aneurysms were idiopathic pseudoaneurysms with a negative diagnostic evaluation for secondary causes. These pseudoaneurysms were treated conservatively; 2 patients did well and 1 patient passed away from severe intracranial vasospasm. Two aneurysms resolved on diagnostic angiogram, and 1 aneurysm was absent on initial angiogram and appeared on follow-up diagnostic imaging 3 months later. Spinal aneurysms are rare neurovascular pathologies that should be considered in the setting of spinal and/or posterior fossa subarachnoid hemorrhage. Conservative treatment may be a potential safe alternative to interventional treatment. Before the initiation of surgical or endovascular treatment, spinal angiography should be repeated because of the potential for spontaneous resolution.

Le Coup de Poignard Rachidien: A Historical Perspective.

A spinal subarachnoid hemorrhage (SAH) is uncommon. One of the earliest detailed analyses of a spinal SAH was in 1928 by the French physician Paul Michon, who coined the term “le coup de poignard rachidien” to describe the pathognomonic, intense spinal pain experienced by patients with spinal SAH, equating it to being stabbed by a dagger. Michon sub-classified spinal SAH into the upper and lower forms, pointing out that the stabbing spinal pain is more characteristic of SAH in the cervical and thoracic regions and especially in the interscapular region. Translation and subsequent analysis of Michon’s original French paper published in La Presse Medicale in 1928 shed light on two cases in which patients presented with le coup de poignard rachidien and signs of spinal cord dysfunction but little, if any, intracranial symptoms. The patients both showed symptomatic relief following therapeutic lumbar puncture. Later, authors have questioned the notion that intense spinal or interscapular pain is mandatory in the diagnosis of spinal SAH and have additionally provided evidence contrary to Michon’s assertion that intracranial symptoms, if any, occur later in the progression of spinal SAH and are largely insignificant.

The Important Liaison Between Onuf Nucleus–Pudendal Nerve Ganglia Complex Degeneration and Urinary Retention in Spinal Subarachnoid Hemorrhage: An Experimental Study

The Adamkiewicz artery (AKA) supplies pudendal nerve roots and conus medullaris. The aim of this study was to elucidate if there is any relationship between neurodegenerative changes of the Onuf nucleus (ON)-pudendal nerve ganglia complex secondary to vasospasm of the AKA after spinal subarachnoid hemorrhage (SAH). This study was conducted on 22 rabbits, which were randomly divided into 3 groups: control (n=5), sham (n= 5), and spinal SAH (n= 12). Experimental spinal SAH was induced at the L2 level. After 2 weeks, the ON-pudendal nerve ganglia complex and AKA were examined histopathologically. Bladder volume values were estimated, and results were analyzed statistically. Two animals died within the first week of experiment. Histopathologically, severe vasospasm of the AKA and neuronal degeneration and neuronal apoptosis were observed in the ON-pudendal nerve ganglia complex in 5 animals of the SAH group. The mean volume of the imaginary AKA, mean bladder volumes, and degenerated neuron densities of ON and pudendal nerve ganglia were estimated. We found that vasospasm of the AKA led to numerous neuron degenerations in ON and pudendal ganglia and consequently urinary retention (P < 0.005). ON-pudendal nerve ganglia complex degeneration secondary to vasospasm of the AKA may be a cause of urinary retention after spinal SAH.

Solitary Ruptured Aneurysm of the Spinal Artery of Adamkiewicz with Subarachnoid Hemorrhage

Spinal subarachnoid hemorrhage (SAH) due to solitary spinal aneurysm is extremely rare. A 45-year-old female patient visited the emergency department with severe headache and back pain. Imaging studies showed cerebral SAH in parietal lobe and spinal SAH in thoracolumbar level. Spinal angiography revealed a small pearl and string-like aneurysm of the Adamkiewicz artery at the T12 level. One month after onset, her back pain aggravated, and follow-up imaging study showed arachnoiditis. Two months after onset, her symptoms improved, and follow-up imaging study showed resolution of SAH. The present case of spinal SAH due to rupture of dissecting aneurysm of the Adamkiewicz artery underwent subsequent spontaneous resolution, indicating that the wait-and-see strategy may provide adequate treatment option.

Subarachnoid Hemorrhage from a Thoracic Radicular Artery Pseudoaneurysm after Methamphetamine and Synthetic Cannabinoid Abuse: Case Report

Background Context Isolated spinal artery aneurysms not associated with vascular malformations are exceedingly rare. Purpose To present a rare case of subarachnoid hemorrhage after thoracic radiculomedullary artery pseudoaneurysm rupture in a patient who abused synthetic cannabinoids and methamphetamines. Study Design Case report. Methods A 41-year-old man with a history of polysubstance abuse presented with acute-onset headache, back pain, and transient bilateral lower-extremity numbness. He reported daily use of the synthetic cannabinoid “Spice.” He denied use of other illegal drugs, but laboratory testing was positive for methamphetamines. Magnetic resonance imaging showed a focal hematoma at T2–3, and spinal angiography was negative for vascular abnormalities; however, a follow-up angiogram 6 days later revealed interval development of an irregular dilation of the left T3 radiculomedullary artery originating from the left supreme intercostal artery. Results Surgical trapping and resection of the lesion yielded a good clinical outcome. Conclusions Although two previous case reports have described patients with thoracic radiculomedullary pseudoaneurysm causing spinal subarachnoid hemorrhage (SAH), this is the first reported case associated with synthetic cannabinoids and methamphetamine abuse. Although this diagnosis is exceptionally rare, clinical presentation of SAH with associated back pain and lower-extremity symptoms warrants an aggressive imaging workup. Even in the setting of negative angiography, repeat cerebral and spinal angiograms may be necessary to identify a potentially treatable cause of spinal SAH.

Spinal subarachnoid hemorrhage due to ruptured solitary aneurysm at thoracolumbar level with fatal outcome

Sirs: Spinal subarachnoid hemorrhage (SAH) acounts for less than 1% of SAHs. Cerebral complications are uncommon and moderate in severity. We report on a 30year old woman suffering from severe cerebral vasospasms, without subarachnoid blood in successive cranial CT scans, due to spinal SAH caused by a ruptured solitary spinal aneurysm of unknown etiology. The patient suffered from a graft-versus-host reaction of her transplanted kidney. Under immunosuppression, she developed recurrent pneumonias and a septicemia with unknown germ that were treated by intravenous antibiotics. In the further course, she suddenly presented with headache, back pain and progressive behavioural disturbances. Cranial CT at this time was normal. Three lumbar punctures revealed a hemorrhagic CSF that was considered to be artificially bloody. Because of increasing paraparesis and rectal incontinence, the patient was referred to our clinic one week later. On admission, she was in poor clinical condition with reduced consciousness, no speech production, nuchal rigidity and paraplegia lasting for more than 24 hours. Cranial CT was normal, whereas cranial MRI showed bilateral MCA-infarction on diffusionweighted MRI (Fig. 1A). Spinal MRI revealed a ventrally located intraspinal circular tumour at the level of the twelfth thoracic vertebra with an intradural T1-hyperintensive signal in the thoracolumbar canal (Fig. 1B). Suboccipital puncture yielded a hemorrhagic CSF (2540 cells per ll). Conventional panangiography revealed a solitary aneurysm (8 · 15 mm) originating from the descending branch of the anterior spinal artery at the level of the twelfth thoracic vertebra (Fig. 1C) as well as generalised, severe cerebral vasospasms. Despite immediate triple-Hand nimodipine-therapy, CT 12h later demonstrated large bilateral MCAinfarction, but was still without any cerebral SAH (Fig. 1D). Because of the infavorable prognosis, palliative treatment was carried out until death due to a pneumogenic sepsis 23 days later. To date, 20 cases of spinal SAH due to a rupture of isolated spinal aneurysms have been reported [1–2, 4–16]. Of the eight reported patients with thoracolumbar aneurysms, all had an acute onset of pain in the thoracolumbar region [1, 8, 11, 13, 15]. Three also had paraparesis [1, 8]. Six of the eight patients were treated surgically [8, 11, 13, 15] whilst the other two had a conservative treatment [1]. All patients recovered either without or with minor neurological deficits. The authors found two dissecting aneurysms [8], an inflammation within the vessel wall in two cases [1, 11] and no evident etiology in the other four reports [1, 8, 13, 15]. In our patient, general autopsy did not reveal any underlying systemic (e.g. polyarteriitis nodosa, connective tissue disorder, syphilis), cerebral or further spinal vascular pathology. Since the SAH was related in timing to systemic infection in the context of immunosuppression, the aneurysm may result from a local inflammation. Morphologically, inflammatory aneurysms are characterised by proliferation of the tunica intima and media as well as inflammatory infiltrates. Infectious agents may be detected within the vessel wall [4, 11]. However, the aneurysm in our patient only yielded a prominent fibroblastic proliferation without inflammatory infiltrates (Fig. 2). Additional analysis of blood and CSF samples did not contain any germs and all serological tests were negative. Thus the inflammatory etiology remains speculative. In summary, we present the case of a young woman who suffered from symptomatic cerebral vasospasms due to spinal SAH caused by a ruptured solitary spinal aneurysm. Pathogenesis of cerebral vasospasm is unclear, but is most probably due to a distant inflammatory response caused by the subarachnoid blood [3]. Although there have been a few R. Surges AE M. Schubert AE C. Weiller A. Hetzel AE W.-D. Niesen (&) Dept. of Neurology University Clinics of Freiburg Breisacherstr. 64 79106 Freiburg, Germany Tel.: +49-761/270-5157 Fax: +49-761/270-5328 E-Mail: wolf-dirk.niesen@uniklinikfreiburg.de

Spinal subarachnoid hemorrhage complicating oral anticoagulant therapy

Spinal subarachnoid hemorrhage (SAH) is rare clinical entity possible owing to the diluting and fibrinolytic effects of cerebrospinal fluid (CSF). When it occurs, it is most commonly encountered in the thoracic segment of the subarachnoid space. We present a case of a 50-year-old man who sustained spinal SAH in the cervical and thoracic segments related to anticoagulant therapy. He progressed to significant neurological deficit since he was inoperable, an observation that supports the need for decompression surgery. We should be aware of potential hematomyelia should a patient on anticoagulant therapy develop neurological symptoms localized to the spinal cord. When available, magnetic resonance (MR) imaging is the modality of choice to diagnose and follow-up spinal SAH.