Posterior realignment of basilar invagination with facet joint distraction technique.

PURPOSE: We describe our experience with management of basilar invagination (BI) with the atlantoaxial dislocation (C1/C2) joint reduction technique, including posterior atlantoaxial internal fixation. MATERIALS AND METHODS: From 2008 to 2018, eleven patients with atlantoaxial dislocation (AAD) and BI underwent surgical reduction using C1/C2 the joint reduction technique with a fibular graft/peek cage placement followed by C1 lateral mass/C2 pedicle screw fixation. In two cases that we originally planned to perform C1/C2 joint reduction, occiput-C2 pedicle screw fixation was performed instead due to intraoperative challenges. Post-operative course and surgical complications will be discussed. RESULTS: A total of 13 patients, with an average age of 30.46 ± 13.23 years (range 12-57), were operated. In one patient, iatrogenic vertebral artery injury occurred without any neurological complication. JOA score improved from 10.45 ± 1.128 to 15.0 ± 1.949 (p < 0.0001, paired t-test). All radiological indices were improved (p at least < 0.001). No construct failure was seen in any of the patients with C1-2 facet joint distraction technique during follow-up, and no additional anterior decompression surgery was required. CONCLUSIONS: C1/C2 joint reduction technique with fibular graft/cervical PEEK cage of BI patients together with AAD seems to be an effective and safe surgical method of treatment.

What is the restorative effect of VEGF inhibitor bevacuzimab against subarachnoid hemorrhage in an experimental model?

BACKGROUND: This study investigated the effect of vascular endothelial growth factor (VEGF) inhibitor bevacuzimab (BVZ) on the rabbit basilar artery using an experimental subarachnoid hemorrhage (SAH) model. METHODS: Eighteen adult male New-Zealand white rabbits were randomly divided into three groups: a control group (n = 6), SAH group (n = 6), and SAH+BVZ group (n = 6). Experimental SAH was created by injecting autologous arterial blood into the cisterna magna. In the treatment group, the subjects were administered a daily dose of 10 mg/kg, intravenous BVZ for 2 days after the SAH. Basilar artery diameters were measured with magnetic resonance angiography (MRA) 72 h after the SAH in all groups. After 72 h, whole brains, including the upper cervical region, were obtained from all the animals after perfusion and fixation of the animal. The wall thickness, luminal area, and the apoptosis at the basilar arteries were evaluated in all groups. RESULTS: BVZ significantly prevented SAH-induced vasospasm confirmed in vivo with MRA imaging with additional suppression of apoptosis on basilar artery wall. DISCUSSION: VEGF inhibition with BVZ has shown to have a vasospasm and apoptosis attenuating effect on basilar artery in a SAH model.

Contributions of 12/15-Lipoxygenase to Bleeding in the Brain Following Ischemic Stroke.

Ischemic strokes are caused by one or more blood clots that typically obstruct one of the major arteries in the brain, but frequently also result in leakage of the blood-brain barrier and subsequent hemorrhage. While it has long been known that the enzyme 12/15-lipoxygenase (12/15-LOX) is up-regulated following ischemic strokes and contributes to neuronal cell death, recent research has shown an additional major role for 12/15-LOX in causing this hemorrhagic transformation. These findings have important implications for the use of 12/15-LOX inhibitors in the treatment of stroke.

Gene-Silencing Screen for Mammalian Axon Regeneration Identifies Inpp5f (Sac2) as an Endogenous Suppressor of Repair after Spinal Cord Injury.

Axonal growth and neuronal rewiring facilitate functional recovery after spinal cord injury. Known interventions that promote neural repair remain limited in their functional efficacy. To understand genetic determinants of mammalian CNS axon regeneration, we completed an unbiased RNAi gene-silencing screen across most phosphatases in the genome. We identified one known and 17 previously unknown phosphatase suppressors of injury-induced CNS axon growth. Silencing Inpp5f (Sac2) leads to robust enhancement of axon regeneration and growth cone reformation. Results from cultured Inpp5f(-/-) neurons confirm lentiviral shRNA results from the screen. Consistent with the nonoverlapping substrate specificity between Inpp5f and PTEN, rapamycin does not block enhanced regeneration in Inpp5f(-/-) neurons, implicating mechanisms independent of the PI3K/AKT/mTOR pathway. Inpp5f(-/-) mice develop normally, but show enhanced anatomical and functional recovery after mid-thoracic dorsal hemisection injury. More serotonergic axons sprout and/or regenerate caudal to the lesion level, and greater numbers of corticospinal tract axons sprout rostral to the lesion. Functionally, Inpp5f-null mice exhibit enhanced recovery of motor functions in both open-field and rotarod tests. This study demonstrates the potential of an unbiased high-throughput functional screen to identify endogenous suppressors of CNS axon growth after injury, and reveals Inpp5f (Sac2) as a novel suppressor of CNS axon repair after spinal cord injury. Significance statement: The extent of axon regeneration is a critical determinant of neurological recovery from injury, and is extremely limited in the adult mammalian CNS. We describe an unbiased gene-silencing screen that uncovered novel molecules suppressing axonal regeneration. Inpp5f (Sac2) gene deletion promoted recovery from spinal cord injury with no side effects. The mechanism of action is distinct from another lipid phosphatase implicated in regeneration, PTEN. This opens new pathways for investigation in spinal cord injury research. Furthermore the screening methodology can be applied on a genome wide scale to discovery the entire set of mammalian genes contributing to axonal regeneration.

Genetic ablation and short-duration inhibition of lipoxygenase results in increased macroautophagy.

12/15-lipoxygenase (12/15-LOX) is involved in organelle homeostasis by degrading mitochondria in maturing red blood cells and by eliminating excess peroxisomes in liver. Furthermore, 12/15-LOX contributes to diseases by exacerbating oxidative stress-related injury, notably in stroke. Nonetheless, it is unclear what the consequences are of abolishing 12/15-LOX activity. Mice in which the alox15 gene has been ablated do not show an obvious phenotype, and LOX enzyme inhibition is not overtly detrimental. We show here that liver histology is also unremarkable. However, electron microscopy demonstrated that 12/15-LOX knockout surprisingly leads to increased macroautophagy in the liver. Not only macroautophagy but also mitophagy and pexophagy were increased in hepatocytes, which otherwise showed unaltered fine structure and organelle morphology. These findings were substantiated by immunofluorescence showing significantly increased number of LC3 puncta and by Western blotting demonstrating a significant increase for LC3-II protein in both liver and brain homogenates of 12/15-LOX knockout mice. Inhibition of 12/15-LOX activity by treatment with four structurally different inhibitors had similar effects in cultured HepG2 hepatoma cells and SH-SY5Y neuroblastoma cells with significantly increased autophagy discernable already after 2 hours. Hence, our study reveals a link between ablation or inhibition of 12/15-LOX and stimulation of macroautophagy. The enhanced macroautophagy may be related to the known tissue-protective effects of LOX ablation or inhibition under various diseased conditions caused by oxidative stress and ischemia. This could provide an important cleaning mechanism of cells and tissues to prevent accumulation of damaged mitochondria and other cellular components.

Inhibition of 12/15-lipoxygenase as therapeutic strategy to treat stroke.

Targeting newly identified damage pathways in the ischemic brain can help to circumvent the currently severe limitations of acute stroke therapy. Here we show that the activity of 12/15-lipoxygenase was increased in the ischemic mouse brain, and 12/15-lipoxygenase colocalized with a marker for oxidized lipids, MDA2. This colocalization was also detected in the brain of 2 human stroke patients, where it also coincided with increased apoptosis-inducing factor. A novel inhibitor of 12/15-lipoxygenase, LOXBlock-1, protected neuronal HT22 cells against oxidative stress. In a mouse model of transient focal ischemia, the inhibitor reduced infarct sizes both 24 hours and 14 days poststroke, with improved behavioral parameters. Even when treatment was delayed until at least 4 hours after onset of ischemia, LOXBlock-1 was protective. Furthermore, it reduced tissue plasminogen activator-associated hemorrhage in a clot model of ischemia/reperfusion. This study establishes inhibition of 12/15-lipoxygenase as a viable strategy for first-line stroke treatment.

Following experimental stroke, the recovering brain is vulnerable to lipoxygenase-dependent semaphorin signaling.

Recovery from stroke is limited, in part, by an inhibitory environment in the postischemic brain, but factors preventing successful remodeling are not well known. Using cultured cortical neurons from mice, brain endothelial cells, and a mouse model of ischemic stroke, we show that signaling from the axon guidance molecule Sema3A via eicosanoid second messengers can contribute to this inhibitory environment. Either 90 nM recombinant Sema3A, or the 12/15-lipoxygenase (12/15-LOX) metabolites 12-HETE and 12-HPETE at 300 nM, block axon extension in neurons compared to solvent controls, and decrease tube formation in endothelial cells. The Sema3A effect is reversed by inhibiting 12/15-LOX, and neurons derived from 12/15-LOX-knockout mice are insensitive to Sema3A. Following middle cerebral artery occlusion to induce stroke in mice, immunohistochemistry shows both Sema3A and 12/15-LOX are increased in the cortex up to 2 wk. To determine whether a Sema3A-dependent damage pathway is activated following ischemia, we injected recombinant Sema3A into the striatum. Sema3A alone did not cause injury in normal brains. But when injected into postischemic brains, Sema3A increased cortical damage by 79%, and again, this effect was reversed by 12/15-LOX inhibition. Our findings suggest that blocking the semaphorin pathway should be investigated as a therapeutic strategy to improve stroke recovery.

Extraforaminal Microdiscectomy for Upper Lumbar Disc Herniations: A Minimally Invasive Alternative Surgical Approach.

BACKGROUND: Various methods and techniques have been developed for extraforaminal decompression, particularly for far lateral lumbar disc herniation. Distinct anatomical differences are noticeable in the upper levels of the lumbar spine, which may complicate the related surgical approach. This study aimed to determine the safety and efficiency of the far lateral extraforaminal approach for the upper lumbar disc. METHODS: L1-2 and L2-3 migrated lumbar disc herniations were defined as upper lumbar disc herniations. 31 consecutive patients with upper lumbar disk herniation who underwent extraforaminal lumbar microdiscectomy between January 2018 and March 2022 were retrospectively investigated. The patients were assessed using the interval history, follow-up lower back and leg pain visual analog scale scores (0-100 mm), the Oswestry Disability Index (%), and modified MacNab criteria. RESULTS: 31 consecutive patients with upper lumbar disk herniation (20 men and 11 women) with a mean age of 52.8 ± 10.8 years (range 31-70 years) underwent extraforaminal lumbar microdiscectomy. The preoperative and postoperative visual analog scale scores and Oswestry Disability Index were significantly different (P < 0.001). According to the modified MacNab criteria, 23 patients showed excellent improvement, 5 showed good improvement, and 3 showed fair improvement; thus, the rate of satisfactory improvement was 90.3% at the 2-year follow-up. No patients required reoperation at the operative level during follow-up. CONCLUSIONS: Extraforaminal lumbar microdiscectomy is a safe and effective minimally invasive surgical technique for treating upper lumbar disc herniation.

Study the effects of zonisamide on fine structure of rabbit basilar artery and hippocampus in rabbit subarachnoid hemorrhage model.

BACKGROUND: In this study, we investigated the effect of a novel antiepileptic drug, zonisamide (ZNS), on the basilar artery and hippocampus in a rabbit subarachnoid hemorrhage (SAH) model. METHODS: Three groups of New Zealand white rabbits were used: a sham (non-SAH) group, an SAH + saline group, and SAH + drug treatment group that received ZNS. In the treatment group, the subjects were given ZNS for 3 days after the SAH. Hippocampal sections were evaluated for neural tissue degeneration. Basilar artery lumen areas and arterial wall thickness were also measured in all groups. RESULTS: The mean luminal area of the SAH + ZNS was significantly greater than the SAH + saline group. In addition, the arterial wall thickness of SAH + ZNS group was significantly thinner than the SAH + saline group. The neuronal degeneration scores of the hippocampal CA1 regions in the SAH + ZNS group were significantly lower than the SAH + saline treatment animals. CONCLUSIONS: These results indicate that ZNS has a vasodilatatory effect on the basilar artery and a neuronal protective effect in the CA1 region of the hippocampus in a rabbit SAH model.

An unusual case of pediatric cervical myelopathy due to congenital spinal canal stenosis.

Cervical myelopathy is a condition that is rarely reported in pediatric patients who have movement or neuromuscular disorders. We, herein, present a rare case of cervical myelopathy observed in a 14-year-old patient, who was previously a healthy boy treated with cervical laminoplasty, which was caused by cervical spinal canal stenosis based on multiple level disc herniation. The patient presented to the clinic with spastic and ataxic gait with previous diagnostic challenges. Magnetic resonance imaging showed cervical degenerative changes mainly marked at the C3-C4 and C4-C5 levels, along with canal narrowing and a central high signal cord abnormality on T2-weighted images. A C3-C4 open-door laminoplasty surgery technique was performed. The neurological symptoms and signs improved dramatically following surgery. Subsequently, cervical computed tomography and magnetic resonance imaging showed good decompression of the cervical spinal cord during the 5 years of follow-up with the preservation of the range of movement. We concluded that though it is pretty rare, cervical myelopathy should be considered in diagnosing adolescent patients with gait and balance disorders.

Salvage posterior atlantoaxial fixation techniques: A retrospective study.

OBJECT: Since the atlantoaxial region have critical neurovascular anatomy and limited bone surface for fusion, the application and choice of salvage fixation techniques are highly important. To discuss alternative posterior atlantoaxial fixation surgery techniques. METHODS: We retrospectively surgical records of 22 patients that posterior atlantoaxial fixation techniques were applied. RESULTS: The patients included 11 males and 11 females (mean age: 65.7 years). The fracture type that caused instability is type 2 odontoid fractures (22). In six of these patients alternative stabilization techniques were applied due to anatomical variations, huge venous bleeding and iatrogenic trauma of the screw entry points during surgery. CONCLUSIONS: Owing to anatomical variations, intraoperative challenges, and/or instrumentation failures, performing alternative surgical fixation technique is an important factor that affects the success of stabilization of the atlantoaxial region. Knowledge of salvage techniques especially during the learning curve is vitally important. Surgeons should adapt to intraoperative surgical challenges as required.

Morphometric measurements of safety zones and orientation angles for freehand placement of revision screws in atlas lateral mass.

AIM: To demonstrate the possibility of revision screw placement to the atlas, as well as define the safety zones and orientation angles. MATERIAL AND METHODS: This retrospective study analysed the records of four patients who were operated for AAI earlier. Because they needed revision of Atlas screws, they were re-operated after obtaining the measurements mentioned in this study. In addition, measurements of 50 healthy subjects were included in the study as the control group. Maximum screw lengths were also measured. RESULTS: Safe zone in the ideal sagittal direction were wider. As the screw projection becomes more cephalic direction in the sagittal plane, the safe zone for the screw becomes narrower. With the sagittal angle moving forwards cranially, the screw length becomes longer. CONCLUSION: Atlas lateral mass screws could be safely revised whenever needed. The fact that needs to be considered is that the angular range becomes narrower, and the screw length becomes longer when the screw is directed more cranially.

Azathioprine as a Neuroprotective Agent in Experimental Traumatic Spinal Cord Injury.

AIM: To evaluate the protective effects of azathioprine, a macrophage-inhibiting agent, on secondary injury in spinal cord trauma. MATERIAL AND METHODS: A total of 40 Wistar rats were randomly divided into 4 groups. All the animals had undergone T8-10 laminectomy. Except in group I (control), all the animals were exposed to spinal cord trauma at the T9 level. Animals in group II (trauma) received no treatment following trauma. Animals in group 3 (treatment) and group IV (vehicle) were given intraperitoneal azathioprine 4 mg/kg and saline 2 ml, respectively, 30 minutes after the trauma. Half of the animals in each group were sacrificed 24 hours after injury and specimens were used for biochemical and immunohistochemical evaluations. The rest of the animals were followed-up for 4 weeks in terms of neurological functions and were also sacrificed to perform the histopathological analysis. RESULTS: Significant decrease in apoptotic cells and improved neurological function were observed in the animals treated with azathioprine. Biological and immunohistochemical analysis also showed less oxidative stress in this group compared to those without treatment. CONCLUSION: Azathioprine, a potent macrophage-inhibiting agent, has been shown to decrease the extent of secondary injury following spinal cord trauma.

Comparison of the effect of mexiletine and methylprednisolone on neural function and histopathological damage after transient spinal cord ischemia in rabbits.

AIM: The purpose of this study was to investigate the effect of mexiletine on the neural function and histopathological changes after ischemic spinal cord injury in rabbits. We also compared the effect of mexiletine to that of methylprednisolone. MATERIAL AND METHODS: Twenty six male New Zealand white rabbits were randomly divided into six groups. Group 1; sham operated group (n=3) underwent only the surgical exposure of infrarenal aorta. Group 2 (n=4) received neither intravenous (iv) nor intraperitoneal medication but the infrarenal aorta was cross-clamped. Group 3 (n=5) received intravenous infusion of 20 ml/kg/h normal saline. Group 4 (n=5) received 30 mg/kg intravenous methylprednisolone. Group 5 (n=3) received intraperitoneal 20mg/kg/h normal saline. Group 6 (n=6) received 50mg/kg mexiletine intraperitoneally. Temporary spinal cord ishemia was induced by infrarenal aortic occlusion for 25 minutes and followed by reperfusion. The neural status was scored using the Tarlov criteria at 24 hours after reperfusion. Immediately after the neurological scoring, the spinal cords of all animals were removed for histopathological study. RESULTS: Histopathological examination scores were significantly higher in group 6 compared to group 2 (p < 0.05). CONCLUSION: Mexiletine can significantly ameloriate the neural function and prevent histopathological damage after transient spinal cord ischemia in rabbits. This is the first research that investigates the neuron=protective effect of mexiletine in a spinal cord ischemia model.

Topiramate attenuates hippocampal injury after experimental subarachnoid hemorrhage in rabbits.

OBJECTIVE: The aim of this study was to investigate the ability of topiramate (TPM) to prevent neural injury in a rabbit model of subarachnoid hemorrhage (SAH). The effect of TPM on cerebral vasospasm was also evaluated. METHODS: Fifty-three New Zealand white rabbits were allocated into three groups randomly. SAH was induced by injecting autologous blood into the cisterna magna. The treatment groups were as follows: (1) sham operated (no SAH (n=18); (2) SAH only (n=17); (3) SAH + TPM (n=18). Hippocampal sections were evaluated for neural tissue degeneration, using the previously described neural degeneration scoring system. The ApopTag peroxidase in situ apoptosis detection kit (Serologicals Corp., former Intergen) was used to assess apoptosis in the hippocampal sections and the effect of TPM on the apoptotic response. Basilar artery lumen areas and arterial wall thickness were also measured in all groups. RESULTS: There was a statistically significant difference between the mean degeneration scores of the control and SAH only groups (p<0.05). The level of neural degeneration in TPM treated group was significantly lower compared with SAH only group (p<0.05), but not significantly higher than the control group (p>0.05). There were no statistically significant differences between arterial cross-sectional area and arterial wall thickness measurements of the SAH group and SAH + TPM group. CONCLUSION: These findings demonstrate that TPM has marked neuroprotective effect in an experimental model of SAH in rabbits. This observation may have clinical implications suggesting that this antiepileptic drug could be used as a possible neuroprotective agent in patients without major adverse effects.

Delayed pseudomyelomeningocele: a rare complication after foramen magnum decompression for Chiari malformation.

BACKGROUND: A variety of complications after FMD with or without duraplasty for Chiari malformation have been described. Although cerebellar ptosis through the dural opening and pseudomeningocele are well-known rare complications of this procedure, spinal cord herniation manifesting as pseudomyelomeningocele formation has not previously been cited in the literature. In this report, we present a case of delayed pseudomyleomeningocele after FMD. CASE DESCRIPTION: A 22-year-old man presented with progressive spinal cord compression symptoms 7 years after undergoing FMD for Chiari malformation. Craniocervical MRI of the patient revealed pseudomyelomeningocele at C1 level together with cord distortion. The patient underwent untethering surgery for spinal cord adhesions; neural tissue was freed microsurgically from the adjacent structures and duraplasty was performed with synthetic graft. In the early postoperative period, his symptoms resolved moderately. CONCLUSION: Neural tissue shift including the spinal cord through the dural opening may occur after a large posterior fossa decompression without duraplasty for Chiari malformation. Postoperative inadequate CSF circulation due to arachnoid scarring around the decompression area may facilitate this type condition. Early diagnosis of such a complication is of vital importance to prevent serious neurologic deficits, and release surgery with proper duraplasty and also restoration of CSF circulation is the choice of treatment.

Ideal screw entry point and projection angles for posterior lateral mass fixation of the atlas: an anatomical study.

Although various posterior insertion angles for screw insertion have been proposed for C1 lateral mass, substantial conclusions have not been reached regarding ideal angles and average length of the screw yet. We aimed to re-consider the morphometry and the ideal trajections of the C1 screw. Morphometric analysis was performed on 40 Turkish dried atlas vertebrae obtained from the Department of Anatomy at the Medical School of Ankara University. The quantitative anatomy of the screw entry zone, trajectories, and the ideal lengths of the screws were calculated to evaluate the feasibility of posterior screw fixation of the lateral mass of the atlas. The entry point into the lateral mass of the atlas is the intersection of the posterior arch and the C1 lateral mass. The optimum medial angle is 13.5 +/- 1.9 degrees and maximal angle of medialization is 29.4 +/- 3.0 degrees . The ideal cephalic angle is 15.2 +/- 2.6 degrees , and the maximum cephalic angle is 29.6 +/- 2.6 degrees . The optimum screw length was found to be 19.59 +/- 2.20 mm. With more than 30 degrees of medial trajections and cephalic trajections the screw penetrates into the spinal canal and atlantooccipital joint, respectively. Strikingly, in 52% of our specimens, the height of the inferior articular process was under 3.5 mm, and in 70% was under 4 mm, which increases the importance of the preparation of the screw entry site. For accommodation of screws of 3.5-mm in diameter, the starting point should be taken as the insertion of the posterior arch at the superior end of the inferior articular process with a cephalic trajection. This study may aid many surgeons in their attempts to place C1 lateral mass screws.

Functional and clinical evaluation for the surgical treatment of degenerative stenosis of the lumbar spinal canal.

OBJECT: This study was designed to evaluate the efficacy of decompressive surgery for degenerative lumbar spinal stenosis (LSS) on a functional and clinical basis. METHODS: A prospective analysis and follow-up of 125 consecutive patients with degenerative LSS between 2000 and 2006 were performed. All patients underwent surgery for lumbar stenosis. Functional evaluations of the patients were performed using a treadmill, the visual analog scale, and the Oswestry Disability Questionnaire (ODQ). These parameters were recorded before surgery and the 3rd month and 1st and 2nd years after treatment. The first symptom time (FST), maximal walking duration (MWD), and thecal sac cross-sectional area (CSA) before and after surgery were also recorded. Statistical relations between variables were calculated. RESULTS: As patient ages increased, the CSA of the thecal sac decreased. Decompressive surgery reached the target according to the difference between the preoperative and postoperative thecal sac CSA. A correlation between the CSA of the thecal sac and FST, and between the CSA of the thecal sac and MWD could not be established. There was a significant correlation between the FST and MWD, and a negative correlation could be established between the MWD and the ODQ score. Surgery led to significant decreases in the ODQ score. Maximal improvement was observed in the 3rd month after decompressive surgery. CONCLUSIONS: The treatment for LSS should be decided using functional criteria; radiological criteria may not correlate with the severity of the disease. Improvements following lumbar decompression surgery continued within 1 year of treatment according to the ODQ and did not change significantly thereafter.

Circumferential total resection of cervical tumors: report of two consecutive cases and technical note.

To date, few studies have addressed the subaxial vertebrectomy technique and related anatomical landmarks in this method. Total spondylectomy is performed via piecemeal resection or en bloc removal in a one-stage procedure associated with stabilizing the spine and preserving neurological status. In this presentation, a circumferential total cervical tumor resection for subaxial cervical spine lesions was described. Two cases of subaxial cervical malignancy, one with primary C3 chondrosarcoma and the other with C4 lung adenosarcoma metastasis, were both treated by the anterior-posterior approach. The lesions could be removed macroscopically totally in both cases. The patients did well after surgery with preserved neurological status and they survived a considerable period without tumor recurrence. Subaxial total tumor resection can be performed safely while preserving vertebral arteries with adequate anatomical knowledge and careful surgical planning, and circumferential vertebrectomy (even intralesional) can provide a long recurrence-free survival period for patients suffering from subaxial spine tumors.

Crossed Wernicke's aphasia after aneurysmal subarachnoid hemorrhage: a case report.

Crossed aphasia (CA) refers to aphasia occurring after right brain damage in right handers. In the literature, numerous CA cases following cerebral ischemia have been reported, but few met the criteria for a prompt diagnosis. The authors present the case of a 52-year-old woman with SAH caused by a right middle cerebral artery (MCA) saccular aneurysm who developed non-fluent aphasia characterized by reduced verbal output, word-finding disturbances and phonemic paraphasias in both oral and written language. 99mTc-HMPAO SPECT was also consistent with right parieto-temporal and frontoparietal ischemia with crossed cerebellar diaschisis on the right cerebellum. A diagnosis of CA was made. One year follow-up showed improvement in communication skills but persistent right fronto-temporo-parietal ischemia. Cerebral vasospasm after aneurysmal SAH symptomatology may vary from motor and sensory disturbances to cognitive disabilities. Aphasia developing after cerebral ischemia of the right hemisphere in a right-hand dominant patient following vasospasm may be a misleading symptom for the localization of the insult. Keeping a high index of suspicion may help in making the correct diagnosis. The changes in the perfusion patterns of cerebellum as assessed by SPECT study during the acute and recovery phases suggests the involvement of cerebellum in language functions.