Transient Focal Neurological Deficits Research Articles

Iatrogenic cerebral amyloid angiopathy and Alzheimer's disease co-pathology.

Iatrogenic cerebral amyloid angiopathy, a disease caused by contact with neurosurgical material or human growth hormone contaminated by beta-amyloid peptide (Aβ), has a prion-like transmission mechanism. We present a series of three patients under 55 years of age who underwent cranial surgery. All of them developed multiple cerebral hemorrhages, transient focal neurological deficits, and/or cognitive impairment after 3-4 decades. MRI was compatible with CAA, and Aβ deposition was confirmed. The third patient, who had a ventriculoperitoneal valve, also showed Aβ deposition in the peritoneum and diagnostic biomarkers of Alzheimer's disease. Co-pathology with Alzheimer disease and its iatrogenic transmission should be considered.

Abstract 126: Bilateral Limb Shaking TIA secondary to Severe Bilateral Carotid Stenosis

Introduction A case describing bilateral limb shaking episodes in a patient with severe bilateral carotid disease ‐ a rare manifestation of limb‐shaking TIA. Methods '‐ Results CASE A 71‐year‐old male patient with a past medical history significant for type 2 diabetes mellitus and bilateral carpal tunnel syndrome is being followed for symptomatic management of known axonal sensorimotor diabetic polyneuropathy in the neuromuscular clinic. He reported on one of his follow‐up visits that he had been experiencing an eight‐month history of presyncopal to syncopal events occurring solely in the standing position, not followed by postictal state but amnesia to the syncope itself, and resulting in falls with mild injuries. He was experiencing new‐onset dry eyes and mouth but denied anhidrosis or early satiety, and cardiac event monitoring during one of these events was unremarkable for rhythmic causes. Examination was unchanged from previously and was significant for findings consistent with length‐dependent sensory loss with hyporeflexia/areflexia. The constellation of symptoms was suggestive of autonomic dysfunction, and while this may be seen with diabetic polyneuropathy, workup for alternative autonomic neuropathies (including SSA/SSB antibodies, paraneoplastic antibody panel, serum protein electrophoresis with immunofixation, serum free light chains, transthyretin amyloid) was obtained with plan for follow‐up. A few months later, he presented to the ED with intermittent upper extremity shaking (more pronounced on the right than on the left) preceding the syncopal events, which only occurred in the standing position or during physical activity and resolved with rest. There were no (transient) focal neurological deficits, including monocular vision loss or hemispheric syndrome. CTA of the head/neck was obtained and was notable for severe to critical stenoses of the bilateral internal carotid arteries (see figure 1). Duplex US revealed 80‐99% stenosis of both right and left proximal internal carotid arteries. The constellation of findings was most suggestive of bilateral limb‐shaking TIA secondary to bilateral carotid stenosis. He was started on secondary stroke prevention and referred to vascular surgery for evaluation of revascularization. The patient underwent left carotid endarterectomy briefly afterward and experienced resolution of the events – he later also underwent carotid endarterectomy of the right side and remains asymptomatic. DISCUSSION: Limb‐shaking TIA is a well‐described yet underrecognized manifestation of severe carotid disease reported by C.M. Fisher in 1962. The “limb shaking” episodes are typically unilateral, affecting the arm or leg, and are often mistaken for seizures [1]. Pathogenesis involves hemodynamic impairment related to extracranial/intracranial carotid stenosis or occlusion resulting in stereotypical recurrent contralateral limb shaking episodes precipitated by physical activity [2], [3]. The constellation of “limb shaking” spells precipitated upon standing or physical activity with resolution after activity cessation should raise suspicion for limb‐shaking TIA and warrant vascular imaging. Treatment includes medical secondary stroke prevention and revascularization procedures [4], which can alleviate or even resolve the transient symptoms [2]. Conclusion Limb‐shaking TIA is an important yet underrecognized manifestation of relative cerebral hypoperfusion related to severe cerebrovascular disease. This case describes bilateral limb shaking episodes in a patient with severe bilateral carotid disease ‐ a rare manifestation of limb‐shaking TIA.

Expediting the TIA Workup (P6-5.024)

<h3>Objective:</h3> Reduction of length of stay (LOS) for transient ischemic attack (TIA) admissions at a public safety net community hospital. <h3>Background:</h3> Transient focal neurologic deficits are a common chief complaint among patients presenting to Emergency Department (ED). Admitting these patients is costly and increases utilization of limited hospital resources. Thus, the current national trend is to avoid admitting “low risk” TIA patients. The purpose of this study is to design a “TIA pathway,” in a public safety net hospital setting to expedite evaluation of these patients. <h3>Design/Methods:</h3> We based our TIA pathway protocol on work done by Boyle et al. We tailored our protocol, based on the socioeconomic needs of our patients (27.2% uninsured, 5.2% undomiciled), to further improve access to stroke care for our community. With ED collaboration, physician training was performed, including utilization of an order set and understanding guidelines for the TIA pathway and inpatient admission. TIA pathway utilization data and data from admitted TIA patients was gathered from the medical record and AHA Get with the Guidelines registry. In addition, safety data including adverse events, 30 day follow up, readmission, and outcomes were monitored and reviewed monthly by stroke leadership. <h3>Results:</h3> A total of 247 TIA cases were recorded in February 2020 through August 2022. The average LOS of patients admitted to the TIA pathway was 1.58 days, while the average LOS for patients admitted inpatient for TIA workup was 2.92 days. Since the inauguration of TIA pathway, we decreased bed utilization by 130 hospital days. <h3>Conclusions:</h3> A dedicated TIA pathway with well-constructed guidelines, order-sets, and physician education resulted in a significant reduction in hospital LOS for the initial evaluation of TIA patients. Follow up outcome studies will be performed to assess the safety and efficacy of an expedited TIA workup. <b>Disclosure:</b> Dr. Wen has nothing to disclose.

Novel Presentation of Hemiplegic Migraine in a Patient With Cockayne Syndrome

BackgroundCockayne syndrome is a rare DNA repair disorder marked by premature aging, poor growth, and intellectual disability. Neurological complications such as seizures, movement disorder, and stroke have been reported. Hemiplegic migraine has not been reported in association with Cockayne syndrome. MethodsWe report a male with Cockayne syndrome due to biallelic heterozygous pathogenic variants in ERCC6 who presented repeatedly with transient focal neurological deficits and headache, which were consistent with hemiplegic migraine. Two siblings also had Cockayne syndrome and presented with similar symptoms. ResultsOur patient was originally diagnosed based on clinical suspicion and then confirmed by targeted exome analysis of genes associated with Cockayne syndrome. The family's research exome sequencing data were reanalyzed to identify variants in genes known to cause familial hemiplegic migraine. No variants in the genes known to cause familial hemiplegic migraine were identified. ConclusionThis is a novel association of familial hemiplegic migraine in three full siblings with Cockayne syndrome. Hemiplegic migraine has not previously been described as part of the Cockayne syndrome presentation. A separate genetic cause of familial hemiplegic migraines was not identified in an exome-based analysis of genes known to cause this condition. This report may represent an expansion of the Cockayne syndrome phenotype.

Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management.

Cerebral amyloid angiopathy (CAA) is a common untreatable cause of lobar hemorrhages and cognitive decline in the older population. Subset of patients present with its inflammatory subtype with rapid decline in cognitive functions and neurological deficits. Most commonly the underlying pathophysiology of this disease is deposition of insoluble amyloid protein into blood vessel walls which results in vessel fragility leading to local neurotoxicity which may eventually leads to lobar hemorrhages and cognitive decline. The term "Amyloid Spell" encompasses transient focal neurological deficits which is commonly misdiagnosed as seizures or transient ischemic attack in the emergency department. Radiologic findings in these patients may reveal microbleeds, cortical superficial siderosis, white matter hyperintensities, and cerebral edema which support the clinical diagnosis which could be otherwise challenging. CAA diagnostic criteria require CT (Edinburgh Criteria) or MRI imaging, or neuropathology. The diagnosis can be suspected without imaging or neuropathology but cannot be confirmed. This review article provides a critical outlook on different types of presentations, updated diagnostic criteria and management of CAA patients illustrating underlying mechanisms associated with neuronal injury secondary to amyloid deposition.

Beware: Sialadenitis as a Rare Post Neurosurgical Complication: A Single-Institution Clinical Case Series

Acute postoperative sialadenitis is a potentially life-threatening complication of cranial neurosurgery characterized by swelling of the face and neck due to obstruction of salivary ducts by either mechanical obstruction or, potentially, pharmacologic stasis or gland obstruction. Given the paucity of literature surrounding this rare phenomenon, we sought to report our experience with acute sialadenitis after cranial neurosurgery. Retrospective review of patients with acute sialadenitis after neurosurgical craniotomy or craniectomy from a single institution from January 1, 2011, through December 31,2021. Seven patients (median age: 27 years; 6 female) identified meeting our inclusion criteria out of 10,014 patients who underwent craniotomy and/or craniectomy procedures during last 11 years (∼0.006%), 5 of these cases were considered skull base procedures. Five (71%) patients required emergent airway management either via intubation or tracheostomy and 5 (71%) were treated with steroids. Additional supportive care included sialagogues, warm compress, massage, analgesics, and intravenous hydration for all 7 patients. Three patients (43%) developed concomitant transient focal neurologic deficits attributable to the sialadenitis. No mortalities occurred as a result of this complication. Acute post-neurosurgical sialadenitis spans a range of severity, with some patients requiring emergent airway management and prolonged ventilator support whereas other patients only require conservative supportive care. Early recognition of acute sialadenitis after cranial neurosurgery can prevent fatal outcomes and provide complete recovery from this condition. Therefore, all neurosurgeons, anesthesiologists, and intensivists should be aware of this rare, but potentially life-threatening, complication.

Acute prolonged motor aura resembling ischemic stroke after COVID \u2212\u200919 vaccination (CoronaVac): the first case report

BackgroundWe report the first case of a patient who suffered transient focal neurological deficit mimicking stroke following CoronaVac vaccination. However, instead of an ischemic stroke, motor aura was suspected.Case presentationsA 24 year-old Thai female presented with left hemiparesis fifteen minutes after receiving CoronaVac. She also had numbness of her left arm and legs, flashing lights, and headaches. On physical examination, her BMI was 32.8. Her vital signs were normal. She had moderate left hemiparesis (MRC grade III), numbness on her left face, arms, and legs. Her weakness continued for 5 days. A brain CT scan was done showing no evidence of acute infarction. Acute treatment with aspirin was given. MRI in conjunction with MRA was performed in which no restricted diffusion was seen. A SPECT was performed to evaluate the function of the brain showing significant hypoperfusion of the right hemisphere. The patient gradually improved and was discharged.DiscussionsIn this study, we present the first case of stroke mimic after CoronaVac vaccination. After negative imaging studies had been performed repeatedly, we reach a conclusion that stroke is unlikely to be the cause. Presumably, this phenomenon could possibly have abnormal functional imaging study. Therefore, we believed that it might be due to cortical spreading depression, like migraine aura, which we had conducted a literature review.

Can perfusion CT unmask postictal stroke mimics? A case-control study of 133 patients.

To study the diagnostic value of volume perfusion CT (VPCT) in patients with transient focal neurologic deficits following and during epileptic seizures, that mimic symptoms of stroke. A retrospective case-control study was performed on 159 patients who presented with a seizure and received an emergency VPCT within the first 3.5 hours of admission, after being misjudged to have an acute stroke. The reference test was a clinical-based, EEG-supported diagnostic algorithm for seizure. We included 133 patients: 94 stroke-mimicking cases with postictal focal neurologic deficits ("Todd phenomenon," n = 67) or ongoing seizure on hospital admission ("ictal patients," n = 27), and 39 postictal controls without focal neurologic deficits. Patients with Todd phenomenon showed normal perfusion (64%), hypoperfusion (21%), and hyperperfusion (14%) on early VPCT. Ictal patients displayed more hyperperfusion compared to postictal patients (p = 0.015). Test sensitivity of hyperperfusion for ictal patients is 38% (95% confidence interval [CI] 20.7%-57.7%), specificity 86% (95% CI 77.3%-91.7%), positive predictive value is 42% (95% CI 27.5%-58.7%), and the negative predictive value 83% (95% CI 78.6%-86.9%). A cortical distribution was seen in all hyperperfusion scans, compared to a cortico-subcortical pattern in hypoperfusion (p < 0.001). A history of complex focal seizure and age were associated with hyperperfusion (p = 0.046 and 0.038, respectively). VPCT can differentiate ictal stroke mimics with hyperperfusion from acute ischemic stroke, but not postictal patients who display perfusion patterns overlapping with ischemic stroke. This study provides Class IV evidence that VPCT accurately differentiates ictal stroke mimics from acute ischemic stroke.

Hashimoto Encephalopathy: Encephalitis versus Vasculopathy and the Impact of Concussion

Patients with Hashimoto encephalitis may present with seizures, stroke-like episodes, transient focal and global neurological deficits, and a variety of neuropsychiatric disturbances. The encephalopathy evolves with elevated anti-thyroid peroxidase antibodies, independent of hormonal thyroid function. A vasculitic basis is considered in cases that show inflammatory vasculopathy in brain biopsy and postmortem tissues. A relation to autoimmune encephalitis is supported by etiologic localization of the disturbance to vulnerable areas of the mesial temporal lobe and the association of potentially pathogenic antibodies. Both mechanisms presume disruption of the blood-brain barrier. We report a patient with Hashimoto encephalopathy in whom repeated concussions antedated onset of the disorder with overlapping areas of altered brain metabolism and vascular perfusion in the hippocampus, deemed to be most vulnerable in autoimmune encephalopathy and concussive brain injury.

Hashimoto Encephalopathy: Impact of Concussion

Patients with Hashimoto encephalitis may present with seizures, stroke-like episodes, transient focal and global neurological deficits, and a variety of neuropsychiatric disturbances. The encephalopathy evolves with elevated anti-thyroid peroxidase antibodies, independent of hormonal thyroid function. A teenager experienced repeated concussions antedating onset of Hashimoto encephalopathy. Neuroradiological studies showed overlapping areas of altered brain metabolism and vascular perfusion in the hippocampus, deemed most vulnerable in autoimmune encephalopathy. Concussive brain injury may be a contributing factor in the development of encephalopathy due to its capacity to alter the blood-brain barrier.

Cerebral arterio-venous malformations in the paediatric population: Angiographic characteristics, multimodal treatment strategies and outcome

ObjectivesCerebral arterio-venous malformations (AVM) are considered congenital lesions, emerging as an important cause of haemorrhagic stroke in children. The potential influence of age on clinical presentation and angio-architecture have been analysed extensively in the last years. Yet, comparative studies comprising ascending age groups may be limited in their conclusions, especially when comparing young children and adults. It is the aim of this study to evaluate characteristic clinical and angiographic features of AVM within a paediatric subgroup and their correlation to age at presentation. Patients and methodsBetween 1990–2015, 46 children harbouring AVMs were treated at our institution. Clinical presentation, radiological data, treatment strategies and outcome were evaluated retrospectively. ResultsOf 46 consecutive patients, 18 were male and 28 female patients. Mean age was 11.6±4.3years, ranging from 2 to 17 years. 35 patients (76%) presented with haemorrhage. Seizures were found in 6 patients (13%) and progressive or transient focal neurological deficits in 4 individuals (9%). There was one incidental patient, only. Mean age of children presenting with haemorrhage was significantly lower as compared to those without a history of intracranial bleeding (p=0.1). The size of the AVM was small (n=27, 59%), corresponding a grade I AVM in the majority of patients (N=28, 61%). 41 patients (89%) underwent treatment of their AVM by an interdisciplinary approach achieving complete elimination of the lesion in 34 patients (83%). 34 patients (83%) showed at least a favourable outcome (mRS≤2) at last follow-up. An excellent recovery (mRS 0–1) was noted in 28 patients (68%). ConclusionFrom our data we suggest that patients’ age impacts the clinical presentation. Particularly young children seem to bear a higher risk for haemorrhage from their AVM. Treatment of paediatric AVMs can be achieved safely in experienced hands with a high rate of complete elimination and good clinical outcome.

Transient focal neurologic deficits upon hematopoietic stem cell transplantation: just a coincidence?

Transient focal neurologic deficits upon hematopoietic stem cell transplantation: just a coincidence?

Hashimoto’s Thyroiditis and Encephalopathy

Although very rare, the literature describes cases of Hashimoto encephalopathy attesting to its occurrence. Affected patients present with seizures, stroke-like episodes, transient focal and global neurological deficits, and a variety of neuropsychiatric disturbance from dementia to hallucinations and psychosis. The encephalopathy evolves with concomitantly elevated anti-thyroid peroxidase antibodies, independent from hormonal thyroid function setting it apart from thyrotoxicosis and myxedema. A new patient reported with Hashimoto’s encephalopathy, in whom neurocognitive impairment and stroke-like onset of hemiparesis and hemiparkinsonism correlated with brain magnetic resonance imaging fused with positron emission tomography.

Recurrent transient focal neurological deficits in convexity meningioma: TIA or negative motor seizures?

Transient ischemic attack (TIA) is defined as a temporary focal neurological deficit of presumed vascular origin, lasting for less than 1 h, with no evidence of infarct on neuroimaging. If a patient is suffering from multiple cardiovascular risk factors and presents with transient and recurrent focal neurological deficits, the most likely diagnosis considered is TIA. As the possibility of stroke within first 24 h is high, such patients need aggressive investigation and management, and ideally should be hospitalized. TIA usually occurs due to major intracranial or extra cranial artery stenosis. However, if vascular imaging and cardiac workup is normal, possibility of small vessel disease is considered. Space occupying lesions usually presents with seizure, symptoms of raised intracranial pressure or progressive neurological deficits rather than TIA. There are a few case reports where meningioma presented as TIA, due to vascular compromise by encasing internal carotid artery. 1,2 transient focal neurological deficits can have other differentials like post ictal palsy and negative motor seizures. In a given patient with space occupying lesion like meningioma presenting with recurrent transient focal neurological deficits we need to consider all these differentials. We are hereby reporting a case of convexity meningioma, which presented as recurrent focal neurological deficit due to negative motor seizures, mimicking transient ischemic attack.

Abstract W P141: Cerebral Microbleeds and White Matter Hyperintensities as Predictors for Early Stroke Recurrences in Transient Ischemic Attack: Korean TIA eXpression Study

Background: Patients within 24 hours from symptom onset of transient ischemic attack (TIA) are particularly at high risk of early recurrent stroke. Neuroimaging variables are increasingly recognized to help better identify patients at high risk. The Korean TIA eXpression study aimed to determine the risk of early recurrent stroke and its clinical and imaging predictors. Methods: We conducted a hospital-based, multi-center prospective cohort study. TIA was defined by transient focal neurological deficits which result from ischemia and last less than 24 hours. Inclusion criteria were: 1) patients who admitted within 24 hours after symptom onset, 2) those who underwent magnetic resonance imaging and angiography, and 3) age of 45 years or older. We collected baseline data of demographics, vascular risk factors, clinical manifestation, potential mechanism of TIA, neuroimaging findings of acute ischemic lesions, white matter changes, microbleeds, vascular status, and laboratory test results. The primary endpoint was recurrent stroke within 90 days. Results: A total of 500 patients (mean age 64.4, male 58%, mean ABCD2 score 4.3 ± 1.4) were enrolled and completed 90-day follow-up. The primary endpoint of recurrent stroke developed in 25 (5.0%) patients within 90 days. From univariable analyses, we identified the following potential predictors (p &lt; 0.20) of recurrent stroke within 90 days: ABCD2 scores, crescendo TIA, lacunar TIA, symptomatic extracranial occlusion, old lacune, white matter hyperintensities, and cerebral microbleeds. In a multivariable logistic regression analysis, crescendo TIA (adjusted odds ratio (OR) 4.4, 95% confidential interval (CI) 1.3-14.7), lacunar TIA (OR 2.5, 95% CI 1.1-6.1), white matter hyperintensities (OR 2.4, 95% CI 1.1-5.4), and cerebral microbleeds (OR 4.9, 95% CI 1.9-12.8) were independently associated with recurrent stroke within 90 days. Conclusion: In conclusion, the current study suggests that microangiopathy may be a predictor for early recurrent strokes after TIA. Our novel findings need to be validated in future studies.

Stroke warning syndrome: 18 new cases

BackgroundStroke warning syndrome (SWS) is a rare cause of stroke characterized by recurrent and short-lasting episodes of transient focal neurological deficits leading up to infarction. On the basis of clinical findings and neuroimaging, it can be capsular, pontine, or callosal. The aim of this study is to evaluate the prevalence of SWS in patients admitted to our Stroke Unit for an ischemic stroke and to look for the difference in outcome between patients treated or not with systemic thrombolysis by intravenous recombinant tissue plasminogen activator (IV-rtPA). MethodsAmong the 967 patients admitted to our Stroke Unit between April 2008 and January 2013 for ischemic stroke, we identified 18 patients with SWS. Nine patients underwent IV-rtPA (IV Group) and the other 9 (No IV Group) other therapies. ResultsThe prevalence of SWS in our population was 1.8%. The most common risk factors were hypertension and dyslipidemia in both groups. A good outcome at 3-month follow-up (modified Rankin Scale 0–2) was found in 3 patients (33%) in IV Group and in 5 patients (55%) in No IV Group. ConclusionSWS is an under-recognized syndrome. Intravenous rt-PA treatment seems to have lower efficacy than in other subtypes of strokes, but none of the patients with SWS undergoing treatment presented haemorrhagic transformation or other complications.

Cerebellar Ataxia, Hemiplegic Migraine, and Related Phenotypes Due to a CACNA1A Missense Mutation

To document and discuss the broad phenotypic variability in a Portuguese family with cerebellar ataxia, hemiplegic migraine, and related syndromes caused by missense mutation c.1748 (p.R583Q) in the CACNA1A gene. Observational 12-year follow-up study. Community and hospital care. Sixteen patients in a 4-generation family were identified in 1998 in a population-based survey. The follow-up revealed 28 patients (25 of whom were observed) and 32 unaffected relatives with an a priori risk of 50%. Four major phenotypes (migraine with multiple auras, transient focal neurological deficits without headache, coma triggered by minor head trauma, and slowly progressive cerebellar ataxia) were present in various combinations. The initial manifestation was ataxia in 16 patients and a transient episode in 12 patients. Eighteen patients did not have migraine, and 11 showed only ataxia. The c.1748 (p.R583Q) mutation in CACNA1A was confirmed in all 23 of the patients who were tested but was not found in any of the 27 adult relatives. The CACNA1A CAG repeat expansion was excluded. A unique missense mutation in the CACNA1A gene, which exhibits a very high penetrance and expressivity, may present a phenotypic spectrum that is broader than current descriptions. Single-gene disorders can behave as complex traits, which reinforces the importance of genetic modifiers in the tightly regulated function of P/Q-type calcium channels. The clinical spectrum of missense mutation CACNA1A -related disorders is much broader than strictly familial hemiplegic migraine.

Headache with Neurological Deficits and CSF Lymphocytosis: A Meningism and Psychosis Mimic

Headache with neurological deficits and cerebrospinal fluid (CSF) lymphocytosis (HaNDL), a benign condition, known to have confused physicians and neurologists presenting like transient Ischemic Attacks (TIA), central nervous system infections and encephalitis of various etiology. HaNDL is typically seen in young adults, manifested as a triad of headache, transient focal neurological deficits and CSF lymphocytosis. The authors report the case of a 50 -year- old man with episodic headache associated with neck stiffness, altered sensorium and symptoms of acute psychosis. After extensive evaluation including neuroimaging, CSF study, different blood investigations to exclude possible central nervous system infections, autoimmune encephalitis and CNS vascular disease, a diagnosis of HaNDL was arrived. The patient improved with supportive and symptomatic management. HaNDL can present with symptoms akin to meningitis and psychosis. Due caution should be exercised before arrival at the diagnosis of HaNDL, which is a based on exclusion of other life threatening neurologic illness.

Syndrome of Transient Headache and Neurologic Deficits With Cerebrospinal Fluid Lymphocytosis (HaNDL)

The syndrome of transient headache and neurologic deficits associated with cerebrospinal fluid lymphocytosis (HaNDL) is characterized by 1 or more episodes of severe headache, transient neurologic deficits, and lymphocytic pleocytosis in the cerebrospinal fluid. It is a benign and self limited disorder seldom reported in pediatric age. We report the case of a 14-year-old girl who suffered from 2 episodes of headache with transient focal neurologic deficits and pleocytosis consistent with the syndrome of HaNDL. This entity should be taken into account as a differential diagnosis in otherwise healthy children presenting with recurrent headache and acute neurologic deficits. Repeated use of invasive and expensive laboratory and imaging investigations can be avoided when the diagnosis of the syndrome of HaNDL is correctly established.

Transient hemiparesis caused by spontaneous cervical epidural hematoma

Spontaneous cervical epidural hematoma (SCEH) is rare and can result in various clinical phenotypes. Transient focal neurological symptoms, which have not yet been reported on, can result in overlooking this differential diagnosis in patients presenting with passing neurological deficits and assuming the diagnosis of a transient ischemic attack. Therefore, a thorough documentation of patient history is of importance, since this can reveal symptoms suggestive of a different etiology. Here, we present a case of a 66-year-old female who was admitted with a hemiparesis without cortical or cranial neurological abnormalities. When asked for preceding symptoms like headache or neck ache she mentioned interscapular pain. Imaging of the cervical spine showed an epidural hematoma. Symptoms resolved spontaneously over 24 h without surgical intervention. Our case illustrates the variation in the clinical presentation of SCEH which can result in transient symptoms, even without surgical intervention. Therefore, in patients with transient focal neurological deficits this diagnosis should be included in the differential, particularly when cortical and cranial signs are lacking.