Unexplained Neurological Deterioration Research Articles

Post-traumatic Transient Neurological Dysfunction: A Proposal for Pathophysiology.

Unexplained neurological deterioration is occasionally observed in patients with traumatic brain injuries (TBIs). We aimed to describe the clinical features of post-traumatic transient neurological dysfunction and provide new insight into its pathophysiology. We retrospectively collected data from patients with focal neurological deterioration of unknown origin during hospitalization for acute TBI for 48 consecutive months. Brain imaging, including computed tomography, diffusion-weighted imaging and perfusion-weighted imaging, and electroencephalography were conducted during the episodes. Fourteen (2.0%) patients experienced unexplained focal neurological deterioration among 713 patients who were admitted for traumatic intracranial hemorrhage during the study period. Aphasia was the predominant symptom in all patients, and hemiparesis or hemianopia was accompanied in three patients. These symptoms developed within 14 days after trauma. Structural imaging did not show any significant interval change, and electroencephalography showed persistent arrhythmic slowing in the corresponding hemisphere in most patients. Perfusion imaging revealed increased cerebral blood flow in the symptomatic hemisphere. Surgical intervention and anti-seizure medications were ineffective in abolishing the symptoms. The symptoms disappeared spontaneously after 4 h to 1 month. Transient neurological dysfunction (TND) can occur during the acute phase of TBI. Although TND may last longer than a typical transient ischemic attack or seizure, it eventually resolves regardless of treatment. Based on our observation, we postulate that this is a manifestation of spreading depolarization occurring in the injured brain, which is analogous to migraine aura.

Prominent Vessel Signs After Endovascular Thrombectomy Corelates with Unexplained Neurological Deterioration and is a More Reliable Imaging Predictor of Prognosis in Anterior Large Vessel Occlusion Stroke

Fifty percent of patients who undergo endovascular thrombectomy (EVT) for large-vessel occlusion exhibit unfavorable outcomes. The primary factor is attributed to persistent brain impairment even after successful EVT. The prominent vessel sign (PVS) on magnetic resonance susceptibility-weighted imaging reflects the territory of dysmetabolism and may facilitate an expeditious assessment for prognostication. We aimed to examine the relationship between PVS after EVT and the occurrence of early neurological deterioration (END) and 3-month outcomes. Patients who underwent EVT and multimodal magnetic resonance imaging were included. END was defined as an increase of ≥2 in the National Institutes of Health Stroke Scale within 72 hours after EVT. Symptomatic intracranial hemorrhage, malignant edema, and surgical complications were defined as definite END, whereas the other symptoms were categorized as unexplained END (ux-END). The PVS-Alberta Stroke Program Early CT Score (ASPECTS) score was used to evaluate the asymmetric cerebral venous signal on the susceptibility-weighted imaging sequences semiquantitatively. A total of 116 eligible patients were included, 18 (15.5%) of whom presented with ux-END. The 72hour National Institutes of Health Stroke Scale was strongly correlated with diffusion-weighted imaging infarct volume and PVS-ASPECTS and was significantly higher in the ux-END group (16 ± 6 vs. 5 ± 4, P= 0.001). The PVS-ASPECTS score was significantly associated with poor outcomes (odds ratio 2.551, 95% confidence interval (CI) 1.722-3.780, P＜0.001), and PVS-ASPECTS (area under the curve 0.884, 95% CI 0.815-0.953, P<0.001) was superior to diffusion-weighted imaging infarct volume (area under the cure 0.720, 95% CI 0.620-0.820, P= 0.001) in predicting 3-month poor outcome. At the optimal cut-off of 2, the PVS-ASPECT predicted poor outcomes with a sensitivity of 89.7% and a specificity of 78.2%. PVS 72 hours after EVT correlated with ux-END. The PVS-ASPECTS is a more reliable predictor of stroke prognosis and provides valuable information regarding post-EVT management.

Isolated cerebral mucormycosis: A case discussion

We report a case of a 32-year-old male with a history of type 1 diabetes, inhaled drug use, and alcohol use disorder, who presented with encephalopathy, holocranial headaches, neck pain, confusion, and generalized tonic-clonic seizures. The patient initially presented at a rural community hospital with a fever and was found to be in diabetic ketoacidosis (DKA). He was also hemodynamically stable but stuporous, prompting intubation to protect his airway. Despite initial treatment measures, his neurological condition worsened and he remained ventilator-dependent. Key findings include a high glucose level, presence of ketones, and evidence of drug use. Blood cultures showed no growth, but his febrile state persisted. Cerebrospinal fluid (CSF) analysis revealed mild pleocytosis, hyperglycorrhachia but normal protein, with no growth. Neuroimaging showed right hemispheric slowing on EEG and diffusion restriction in the right frontal lobe on MRI. The patient's neurological status worsened on the second day of admission, manifesting as sluggish pupillary reflexes, right third nerve palsy, and decerebrate posturing. Emergent MRI suggested cerebral edema, leading to initiation of hypertonic saline. This case highlights the diagnostic challenges and critical management considerations in a patient with multiple comorbidities presenting with unexplained neurological deterioration, emphasizing the importance of a comprehensive and timely approach to diagnosis and treatment.

Symptomatic Intracranial Hemorrhage after Dural Tear in Spinal Surgery–A Series of 10 Cases and Review of the Literature

Intracranial hemorrhage (IH) after spinal surgery is a rare but potentially life-threatening complication. Knowledge of predisposing factors and typical clinical signs is essential for early recognition, helping to prevent an unfavorable outcome. A retrospective analysis was performed of patients with IH after spinal surgery treated in our institution between 2012 and 2018. The literature dealing with IH complicating spinal surgery was reviewed. Our investigation found 10 patients with IH (6 female and 4 male). To the best of our knowledge, this is the largest series reported so far. The assumable incidence of IH after spinal surgery in our population was 0.0657%. Durotomy was noticed in 6 patients, all of whom were treated according to a local standard protocol. In 4 patients, the dural tear was occult. Hemorrhage occurred mostly in the cerebellar compartment. Eight of 10 patients had long-standing arterial hypertension, which seems to be a risk factor (hazard ratio, 1.58). Five patients were treated conservatively, whereas 3 required a cerebrospinal fluid (CSF) diversion procedure. In 2 patients, revision surgery with duraplasty was necessary. Seven patients were discharged with little to no neurologic symptoms, and 3 had significant deterioration. One patient died because of brainstem herniation. Review of the literature identified 54 articles with 72 patients with IH complicating spinal surgery. Patients with intraoperative CSF loss should be kept under close supervision postoperatively. After opening of the dura, a watertight closure should be attempted. The use of subfascial suction drainage in cases of a dural tear as well as preexistent arterial hypertension seems to be a risk factor for the development of IH. Intracranial bleeding must be considered in every patient with unexplained neurologic deterioration after spinal surgery and should be ruled out by cranial imaging. To ensure early recognition and prevent an unfavorable outcome, a high index of suspicion is required, especially in revision spinal surgery. The treatment is specific to the extent and location of the IH, thus dictating the outcome. In most patients, conservative treatment led to a good outcome. CSF diversion measures may be necessary in patients with compression or obstruction of the fourth ventricle. Large hematomas with mass effect may require decompressive surgery.

Posterior Reversible Encephalopathy Syndrome as a Complication of Induced Hypertension in Subarachnoid Hemorrhage: A Case-Control Study

Induced hypertension (IH) remains the mainstay of medical management for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). However, raising blood pressure above normal levels may be associated with systemic and neurological complications, of which posterior reversible encephalopathy syndrome (PRES) has been increasingly recognized. To ascertain the frequency and predisposing factors for PRES during IH therapy. We identified 68 patients treated with IH from 345 SAH patients over a 3-yr period. PRES was diagnosed based on clinical suspicion, confirmed by imaging. We extracted additional data on IH, including baseline and highest target mean arterial pressure (MAP), comparing PRES to IH-treated controls. Five patients were diagnosed with PRES at median 6.6 d (range 1-8 d) from vasopressor initiation. All presented with lethargy, 3 had new focal deficits, and 1 had a seizure. Although baseline MAP (prior to DCI) did not differ between cases and controls, both MAP immediately prior to IH (112 vs 90) and highest MAP targeted were greater (140 vs 120 mm Hg, both P<.01). Magnitude of MAP elevation was greater (54 vs 34 above baseline, P=.004) while degree of IH was not (37 vs 38 above pre-IH MAP). All 4 surviving PRES patients had complete resolution with IH discontinuation. PRES was diagnosed in 7% of SAH patients undergoing IH therapy, most often when MAP was raised well above baseline to levels that exceed traditional autoregulatory thresholds. High suspicion for this reversible disorder appears warranted in the face of unexplained neurological deterioration during aggressive IH.

Acute Intermittent Porphyria

Acute intermittent porphyria is a metabolic disorder rarely seen in prepubertal children. A delay in diagnosis of acute intermittent porphyria is common because of variable and nonspecific symptoms. We report an 8-year-old boy with right hemimegalencephaly and intractable seizures, who presented with dark-colored urine, hypertension, increasing lethargy, fluctuating seizures, and poor oral intake. He subsequently developed hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion. His urinalysis was negative for red blood cells, and a random urine porphobilinogen level was elevated. Further biochemical and molecular testing confirmed the diagnosis of acute intermittent porphyria. His antiepileptic medications were discontinued and hemin administered, with dramatic clinical improvement. The diagnosis of acute intermittent porphyria was challenging because of his underlying neurologic condition. This case highlights the variable presentation of acute intermittent porphyria and emphasizes the importance of considering the diagnosis even in young patients with underlying neurologic conditions when they present with nonspecific neurovisceral symptoms or with unexplained neurologic deterioration.

Remote cerebellar haemorrhage

Purpose Remote cerebellar haemorrhage is a rare and poorly understood complication of neurosurgery. Methods and results Based on four cases and a literature review of the fifteen last years, we try to describe and analyse this complication Conclusion Remote cerebellar haemorrhage must be considered in patients with unexplained neurological deterioration after cerebral or spinal surgery. Even if mechanism is still unknown venous origin seems obvious. Therefore neurological examination and emergency neuroradiological imaging are needed for patient management.

Remote Cerebellar Hemorrhage after Spinal Surgery

This report details a case of a 56-year-old woman who presented with a herniated lumbar disc at L4-5 with congenital spondylolisthesis (grade II) and developed remote cerebellar hemorrhage following an iatrogenic acute reduction in cerebrospinal fluid (CSF) pressure during spinal interbody fusion. Possible mechanisms are discussed: however, pathological events leading to this complication are unclear. Intracranial hemorrhage (ICH) must be considered in patient presenting with unexplained neurological deterioration not attributable to the spinal surgery, especially when the dura has been opened followed by significant CSF loss. (J Kor Neurotraumatol Soc 2010;6:162-164)

Nonconvulsive Status Epilepticus Causing Prolonged Stupor after Intraventricular Hemorrhage: Report of a Case

We describe the case of an octogenarian woman who experienced a severe alteration of mental state due to non-convulsive status epilepticus (NCSE) complicating an intraventricular hemorrhage. Our report emphasizes that NCSE may be the cause of unexplained neurological deterioration in elderly patients with acute brain injury.

Delayed Emergence from Anesthesia Resulting from Cerebellar Hemorrhage During Cervical Spine Surgery

Cerebellar hemorrhage is an unpredictable complication of spinal surgery. We encountered a case of cerebellar hemorrhage presenting with delayed emergence from anesthesia and hemiplegia after resection of an intradural extramedullar tumor from the cervical spine. Postoperative brain computed tomography revealed hematoma in the cerebellar vermis and right cerebellar hemisphere. The patient made a gradual recovery with conservative treatment. Although the mechanism of cerebellar hemorrhage remains speculative, loss of cerebrospinal fluid may play an important role. Cerebellar hemorrhage must therefore be considered in patients with unexplained neurological deterioration or disturbance on emergence from anesthesia after spinal surgery.

Cerebellar Hemorrhage after Spinal Surgery: Report of Two Cases and Literature Review

Cerebellar hemorrhage remote from the site of surgery may complicate neurosurgical procedures. We describe our experience with two cases of cerebellar hemorrhage after spinal surgery and review the three cases previously reported in the literature to determine whether these cases provide insight regarding the pathogenesis of remote cerebellar hemorrhage. One of our patients developed cerebellar hemorrhage in the vermis and right hemisphere after transpedicular removal of a partially intradural T9-T10 herniated disc with the patient in the prone position. The other patient developed cerebellar hemorrhage in the vermis and bilateral hemispheres after L3-S1 decompression and instrumentation with the patient in the prone position, during which the dura was inadvertently opened. The first patient was treated conservatively and had mild residual dysarthria and gait ataxia 2 months after surgery. The second patient underwent exploration and revision of the lumbar wound with primary dural repair. The cerebellar hemorrhage was treated conservatively, and the patient had mild dysarthria and ataxia 1 month after surgery. Cerebellar hemorrhage must be considered in patients with unexplained neurological deterioration after spinal surgery. Dural opening with loss of cerebrospinal fluid has occurred in every reported case of cerebellar hemorrhage complicating a spinal procedure, supporting the hypothesis that loss of cerebrospinal fluid is central to the pathogenesis of this condition. Because remote cerebellar hemorrhage can occur after procedures with the patient in the supine, sitting, and prone positions, patient positioning seems unlikely to play a causative role in its occurrence.

“Unexplained” Delayed Death From Fungal Meningitis After Meningioma Resection

Progressive deterioration and ensuing death following a neurosurgical procedure often represents a diagnostic challenge to the team responsible for patient care. Many, but not all, causes are treatable if a diagnosis is made early. A 69-year-old woman who died 6 weeks post-operatively following a meningioma resection is reported. An initial routine post-operative course became complicated by progressive neurological deterioration 3-4 weeks later. Despite extensive investigation she died 6 weeks post-operatively without a diagnosis. Autopsy demonstrated extensive Candida meningitis. A review of the literature demonstrates this to be a reported complication in high risk patients, difficult to diagnose, but treatable when identified. Fungal meningitis should be high in the differential diagnosis in the post-operative patient with delayed, unexplained neurological deterioration, especially when associated with negative CSF cultures.

Absence of acidosis in the initial presentation of propionic acidaemia.

The clinical presentation and results of the initial biochemical and haematological investigations in 11 newborn term infants with propionic acidaemia are described. All patients had neurological symptoms. Only four had clinically important acidosis, but all had a raised blood ammonia. A diagnosis of propionic acidaemia should be considered in all newborn infants with unexplained neurological deterioration even in the absence of a metabolic acidosis.

Clinical approach to inherited metabolic diseases in the neonatal period: A 20‐year survey

Every newborn with unexplained neurological deterioration, ketosis, metabolic acidosis or hypoglycaemia should be suspected of having an inherited error of intermediary metabolism. Many of these conditions can be diagnosed clinically with the aid of simple laboratory investigations. Since a substantial number of these diseases respond well to treatment but may otherwise be fatal, and in order to assure adequate prenatal diagnosis in subsequent pregnancies, a high index of suspicion and rapid diagnosis are necessary in the face of the clinical presentations described. According to three major clinical presentations observed in 218 neonates with inborn errors of intermediary metabolism (neurological distress 'intoxication' type, neurological distress 'energy-deficiency' type and hypoglycaemia with liver dysfunction) and according to the proper use of few laboratory investigations, we propose a method of diagnosis which groups these children into five categories. Initial therapy, and sophisticated investigations can be planned on the basis of this grouping.