Multiple Neurological Complications Research Articles

Mycoplasma pneumoniae Infection Presented with Multiple Neurological Complications

Mycoplasma pneumoniae Infection Presented with Multiple Neurological Complications

Primary Human Microglia Are Phagocytically Active and Respond to Borrelia burgdorferi With Upregulation of Chemokines and Cytokines.

The Lyme disease causing bacterium Borrelia burgdorferi has an affinity for the central nervous system (CNS) and has been isolated from human cerebral spinal fluid by 18 days following Ixodes scapularis tick bite. Signaling from resident immune cells of the CNS could enhance CNS penetration by B. burgdorferi and activated immune cells through the blood brain barrier resulting in multiple neurological complications, collectively termed neuroborreliosis. The ensuing symptoms of neurological impairment likely arise from a glial-driven, host inflammatory response to B. burgdorferi. To date, however, the mechanism by which the bacterium initiates neuroinflammation leading to neural dysfunction remains unclear. We hypothesized that dead B. burgdorferi and bacterial debris persist in the CNS in spite of antibiotic treatment and contribute to the continuing inflammatory response in the CNS. To test our hypothesis, cultures of primary human microglia were incubated with live, antibiotic-killed and antibiotic-killed sonicated B. burgdorferi to define the response of microglia to different forms of the bacterium. We demonstrate that primary human microglia treated with B. burgdorferi show increased expression of pattern recognition receptors and genes known to be involved with cytoskeletal rearrangement and phagocytosis including MARCO, SCARB1, PLA2, PLD2, CD14, and TLR3. In addition, we observed increased expression and secretion of pro-inflammatory mediators and neurotrophic factors such as IL-6, IL-8, CXCL-1, and CXCL-10. Our data also indicate that B. burgdorferi interacts with the cell surface of primary human microglia and may be internalized following this initial interaction. Furthermore, our results indicate that dead and sonicated forms of B. burgdorferi induce a significantly larger inflammatory response than live bacteria. Our results support our hypothesis and provide evidence that microglia contribute to the damaging inflammatory events associated with neuroborreliosis.

Neurological complications of lumbar and cervical dural punctures with a focus on epidural injections

Background:Various types of lumbar dural punctures may contribute to neurological injury. The etiologies of dural injury include; inadvertent dural punctures due to epidurals placed for labor anesthesia, epidural steroid injections (ESI/transforaminal TESI; approximately 9 million ESI performed in the US per year), deliberate placement of intradural pain devices, and spontaneous cerebrospinal fluid (CSF) fistulas. Resulting neurological complications may include; spinal headaches/intracranial hypotension, subdural hematomas, and 6th nerve cranial palsies. Furthermore, uniquely in the cervical spine, inadvertent cervical dural punctures attributed to cervcial ESI (CESI) may lead to intramedullary spinal cord injuries (e.g. resulting in monoparesis to quadriplegia) or spinal cord strokes due to intravascular/vertebral artery injections.Methods/Results:In 8 studies, inadvertent lumbar dural punctures contributed to intracranial hypotension, subdural hematomas, and double vision/6th cranial nerve palsies. In 5 of the 6 studies, inadvertent dural punctures occurring during CESI were responsible for intramedullary spinal cord injuries, or direct intravascular/vertebral injections resulting in monoplegia/quadriplegia.Conclusions:Inadvertent lumbar dural punctures led to multiple neurological complications including intracranial hypotension, subdural hematomas, and double vision/6th cranial nerve palsies. Uniquely, inadvertent cervical dural punctures solely due to CESI directly resulted in intramedullary spinal cord injuries or cord stroked and monoplegia/quadriplegia attributed to intravascular/vertebral artery injections. The potential neurological risks/complications/adverse events attributed to lumbar and cervical ESI must be taken into account before spine surgeons and others order these procedures.

Idiopathic intracranial hypertension following varicella zoster infection in a young adult

Abstract Varicella zoster virus (VZV) can present with multiple neurological complications both during and in the immediate post-infectious period. Among these, idiopathic intracranial hypertension (IIH) is a rare but treatable entity exclusively reported in children and adolescents. This report describes a 23 year old female who developed headache and visual disturbances on the third week after the exanthema, who satisfied the diagnostic criteria for IIH. Clinical improvement was achieved with medical management. To the best of our knowledge, this is the first report of IIH in an adult patient following varicella infection.

Antimicrobial-induced cognitive side effects.

Introduction:Antimicrobial-induced cognitive side effects are often overlooked or underreported. Literature often reports symptoms of antimicrobial-induced cognitive impairment under more general blanket terms, such as neuropsychiatric side effects, neurotoxicity, or drug-induced delirium or encephalopathy.Methods:A PubMed search using terms including antibiotics, antifungals, antivirals, antimalarials, side effects, cognitive, neurotoxicity, encephalopathy, and delirium was conducted. Respectively, symptoms of cognitive impairment were teased out of the multiple neurologic complications presented for each case and reported based on antimicrobial class. Articles were excluded if they focused solely on neuropsychiatric side effects such as seizures, psychosis, hallucinations, or mood disturbances, were conducted in animals, or involved antiretroviral medication therapies.Results:Of over 50 case reviews, case reports, retrospective chart reviews, and prospective cohort studies analyzed, 25 were deemed appropriate for purposes of this review. Common antimicrobial-induced cognitive side effects for all antimicrobial classes included confusion, delirium, encephalopathy, and impaired concentration or attention. Recurring risk factors included, but were not limited to, older age and renal impairment. Mechanisms of cognitive impairment were relatively specific to each antimicrobial class.Discussion:Awareness of the potential for antimicrobial-induced cognitive side effects, including the general time frame of symptom onset and symptom presentation, is critical in challenging patient cases. This review article aims to summarize the risk factors, clinical symptoms, mechanisms, and management of antimicrobial-induced cognitive side effects. Pharmacists can play a key role in prevention through adjustment of medications for renal or hepatic dysfunction, avoidance of polypharmacy, and knowledge of critical drug interactions that may precipitate cognitive decline.

The Lyme Disease Spirochete Borrelia Burgdorferi Induces Increased Expression of Multiple Neuroinflammatory Factors in Human Microglial Cells In Vitro

Many microorganisms can cause inflammation in the central nervous system (CNS) by damaging or penetrating the protective blood‐brain and blood‐cerebral spinal fluid barriers that sequester the brain from the periphery. Breakdown of the blood‐brain barrier (BBB) or blood‐cerebral spinal fluid (blood‐CSF) barrier could facilitate entry of both B. burgdorferi and activated immune cells into the CNS leading to multiple neurological complications, collectively termed neuroborreliosis. Indeed, B. burgdorferi has an affinity for the CNS and can be isolated from the CSF of humans as early as 18 days after the bite of an infected tick. However, the mechanism by which the bacterium initiates neuroinflammation leading to neural disfunction remains unknown. The ensuing neurological symptoms are likely a result of a glial‐driven, host inflammatory response to the bacterium. However, the specific contributions of human microglial cells to the pathogenesis of neuroborreliosis have not yet been elucidated.We hypothesize that dead B. burgdorferi and debris persist in the CNS after antibiotic treatment and contribute to an ongoing inflammatory response in the CNS. To begin characterization of this response, highly pure cultures of primary human microglia were incubated with live virulent B. burgdorferi and the membrane lipoprotein Pam3Cys to elucidate the cell‐ and lipoprotein‐specific responses to the bacterium. Cultures were analyzed by immuncytochemistry, real time PCR array and ELISA analysis. Array results were confirmed with individual sets of PCR primers. Our results demonstrate a robust increase in numerous inflammatory chemokines, cytokines and related genes in all treatment conditions examined. Most prominent was an increase in the neurophil chemoattractants IL‐8, IL‐6, CXCL1, CXCL10 and LIF. These data suggest that, in addition to B. burgdorferi, infiltrating phagocytic cells, particularly potentially neurotoxic neutrophils, may be important additional contributors to the early inflammatory events associated with the onset of neuroborreliosis.Our continuing studies are now focused on elucidating microglial phagocytosis of B. burgdorferi using real time PCR arrays and culture monolayers coupled with confocal microscopy and trans emission microscopy. Interestingly, initial data has demonstrated that although no there is no phagocytosis of live bugs in vitro, primary human microglia highly up regulate numerous genes associated with phagocytosis and associated cell signaling when exposed to dead and/or dead‐sonicated forms of B. burgdorferi. More specifically, in microglia exposed to dead and/or dead‐sonicated B. burgdorferi, there was a significant increase in expression of genes known to be involved in recognition of Bb (TLRs, NOD1, CD14); Fc receptors; kinases (LYN, MAPK); and things involved in uptake/phagolysosomes (GULP‐1, members of the Rac/Rho family, phospholipases, VAMP, syntaxin). Taken together, these results suggest that primary human microglia continue to mount a pro‐inflammatory response in the absence of viable Borrelia burgdorferi.Support or Funding InformationThis study was funded by a grant from the University of North Dakota Office of Research Development and Compliance (2014).

Corneal Confocal Microscopy Detects Small Fibre Neuropathy in Patients with Upper Gastrointestinal Cancer and Nerve Regeneration in Chemotherapy Induced Peripheral Neuropathy.

There are multiple neurological complications of cancer and its treatment. This study assessed the utility of the novel non-invasive ophthalmic technique of corneal confocal microscopy in identifying neuropathy in patients with upper gastrointestinal cancer before and after platinum based chemotherapy. In this study, 21 subjects with upper gastrointestinal (oesophageal or gastric) cancer and 21 healthy control subjects underwent assessment of neuropathy using the neuropathy disability score, quantitative sensory testing for vibration perception threshold, warm and cold sensation thresholds, cold and heat induced pain thresholds, nerve conduction studies and corneal confocal microscopy. Patients with gastro-oesophageal cancer had higher heat induced pain (P = 0.04) and warm sensation (P = 0.03) thresholds with a significantly reduced sural sensory (P<0.01) and peroneal motor (P<0.01) nerve conduction velocity, corneal nerve fibre density (CNFD), nerve branch density (CNBD) and nerve fibre length (CNFL) (P<0.0001). Furthermore, CNFD correlated significantly with the time from presentation with symptoms to commencing chemotherapy (r = -0.54, P = 0.02), and CNFL (r = -0.8, P<0.0001) and CNBD (r = 0.63, P = 0.003) were related to the severity of lymph node involvement. After the 3rd cycle of chemotherapy, there was no change in any measure of neuropathy, except for a significant increase in CNFL (P = 0.003). Corneal confocal microscopy detects a small fibre neuropathy in this cohort of patients with upper gastrointestinal cancer, which was related to disease severity. Furthermore, the increase in CNFL after the chemotherapy may indicate nerve regeneration.

Neurological Sequale of Varicella Zoster Virus Infection

Background: Varicella-zoster virus meningoencephalitis is an uncommon complication in immunocompetent adults. Typically, most patients present with neurological symptoms within 7-10 days of onset of rash . Also neurological symptoms preceding the rash or in the absence of the rash are rare. Methods: A 50 year-old female experienced urinary and bowel retention and numbness of heel for three days. She had a painful rash on her right thigh eight weeks earlier. MRI was normal. VZV PCR was positive in the CSF. Her neurological symptoms resolved with Acyclovir. A 23 year-old woman experienced left lower extremity weakness and numbness of right leg and abdomen and urinary retention for one week. She had decreased pin prick in right leg up to T8 level. Serum Hepatitis B and Varicella Zoster virus antibodies were positive. MRI showed restricted diffusion and T2/FLAIR hyperintensity in the pons, mid brain and medial temporal lobe. She was treated with steroids and IVIG. After one month she developed fever, blurry vision and vesicular rash on left forearm. Skin biopsy was positive for Varicella zoster virus antibody. Retinal necrosis was found to be consistent with Varicella zoster virus infection. Patient improved neurologically on Valtrex 1 gm TID. An 84-year-old male had symptoms of severe radicular thoracic pain, urinary and bowel incontinence for one week. MRI of the Thoracolumbar spine showed an intradural, intramedullary enhancing lesion at the T7-T8 level with extensive edema. Autopsy revealed viral encephalomyelitis involving the medulla and multiple foci within the spinal cord with inflammation, necrosis, along with Cowdry viral inclusions consistent with Varicella-zoster virus. Conclusion: The above mentioned cases high light atypical presentation of varicella zoster virus infection.The possibility of varicella zoster virus infection should be considered in patients presenting with un explained myelopathy and restricted diffusion changes, mass lesion or un usual CNS symptoms. Importance: Multiple neurologic complications may follow the reactivation of varicella-zoster virus (VZV), including herpes zoster, vasculopathies, myelitis, retinitis, and zoster sine herpete (pain without rash). Myelitis is one of the rarest neurological complications of vzv infection. Observations: We report three cases of VZV myelitis, two of them were immunocompetent and in two myelitis was associated with concomitant cerebral and brain stem strokes. Conclusions and Relevance: In immunocompetent patient VZV myelitis can manifest in the absence of a rash. Diffusion weighted images on MRI can be normal in the setting of acute myelitis due to VZV infection requiring CSF VZV PCR analysis to make prompt diagnosis and appropriate early treatment can lead to full recovery. Oral treatment for VZV rash does not preclude development of myelitis and may require intravenous antiviral medications to treat the infection subsequently. VZV infection can present as mass lesion of the spinal cord. Concomitant cerebral hemisphere and brain stem ischemic lesions and myelitis can occur due to vzv infection.

Late Onset Neonatal Herpes Encephalitis: A Case-Based CNS Complication and Neurological Outcome

Individual neurological complication caused by Herpes simplex viruses in neonates is well-known. We report neonatal Herpes encephalitis that caused multiple neurological complications in the same patient during acute phase of illness. Our patient differs from previously reported cases in the following ways: 1) Late onset neonatal presentation; 2) Development of multiple neurologic complications during acyclovir therapy; 3) Cesarean-section did not prevent perinatal transmission of Herpes simplex virus; and 4) Our patient’s acute hydrocephalus was managed conservatively and he had no reoccurrence of seizure, hydrocephalus, and no motor deficits. A high degree of suspicion, timely needed supportive medical and surgical care, and prompt initiation of intravenous acyclovir offer the best chance for neurological outcome in neonates with Herpes encephalitis.

Thrombosis of posterior condylar vein with extension to internal jugular vein; a rare radiological finding in traumatic brain injury.

Dear Editor, The posterior condylar canal is located posterior to the occipital condyle and transmits the posterior condylar vein, one of the largest emissary veins in the retromastoid region.[1,6] This vein usually origins from superior bulb of the internal jugular vein or less frequently from the medial side of the distal portion of the sigmoid sinus and connect to the suboccipital venous plexus.[5,9] We report a patient with occipital bone fracture coursing through the posterior condylar canal causing thrombosis of posterior condylar vein with extension to internal jugular vein. To the best of our knowledge, thrombosis of posterior condylar vein with subsequent extension to major venous sinuses due to trauma has not been reported yet. A 50-year-old patient was brought to the emergency department following a fall from 15 steps. Initial head computed tomography (CT) scan demonstrated bilateral inferior frontal hemorrhagic contusions, traumatic subarachnoid hemorrhage in bilateral frontal and right temporal lobe, and linear occipital bone fracture extending to the posterior condylar vein on the right side. There was no extension of fracture line to the major dural venous sinuses. Subsequent CT venography (CTV) demonstrated thrombosis of right posterior condylar vein with extension to upper aspect of right internal jugular vein causing nonocclusive thrombosis [Figure 1]. Given the presence of hemorrhagic brain contusions and nonocclusive nature of thrombosis in the internal jugular vein, patient was not considered an appropriate candidate for anticoagulation and was managed conservatively. Follow-up CTV in 48 h demonstrated stable thrombosis with no extension. Figure 1 Axial CT scan demonstrates linear occipital bone fracture with extension to the right posterior condylar canal (a white arrow). Axial and sagittal oblique CT Venogram (b and c) demonstrate right condylar vein thrombosis (white arrow) with extension to ... Emissary veins connect the extracranial venous system with the intracranial venous sinuses. Although they are usually small in healthy people, they may enlarge in patients with increased intracranial pressure, in patients with high-flow vascular malformations or severe hypoplasia/aplasia or obstruction of the jugular veins. They may also serve as a conduit for retrograde spread of infection or tumors. Familiarity with major posterior fossa emissary veins is important to avoid misdiagnosis as abnormal findings and also to prevent surgical complications, which can result in intracranial hemorrhage, air embolism, and fatal increases in intracranial pressure.[7] The role of traumatic close head injuries as an important etiology of cerebral venous sinus thrombosis has been demonstrated in multiple studies.[2] Extension of skull fractures to venous sinuses had been reported in 10.4% and 13% of patients in two recent large studies.[3,8] Delgado Almandoz et al. demonstrated traumatic dural sinus thrombosis in 40.7% of patients with blunt head trauma with skull fractures extending to dural venous sinuses or jugular bulb, and more than half of those were occlusive.[3] In a more recent study, Rivkin et al. found thrombosis of at least one venous sinus or jugular bulb in 34.9% of patients (20.6% nonocclusive, 14.3% occlusive).[8] Fujii et al. also evaluated 97 patients with skull fractures crossing venous sinuses and found 22.4% of them to have thrombosis.[4] The indication for performing CTV in all of these studies was extension of skull fracture line to the major dural sinuses including superior sagittal sinus, transverse sinus, sigmoid sinus, or jugular bulb, and, to the best of our knowledge, traumatic thrombosis of posterior condylar vein with subsequent extension to major venous sinuses has not been reported yet. Development of venous sinus thrombosis in the setting of blunt trauma can result in poor clinical outcome resulting from multiple neurological complications including increased intracranial pressure, hemorrhagic venous infarctions, and increase in seizure frequency, with mortality rates as high as 50% for occlusive venous thrombosis.[3,4,8] Treatment of dural venous sinus thrombosis in the setting of trauma might be very challenging and only a small minority of patients with occlusive venous sinus thrombosis has been reported in prior studies.[3] In conclusion, in the setting of blunt head trauma, extension of the fracture lines to the posterior condylar canal can cause condylar vein thrombosis with secondary extension to major dural venous sinuses. Increase in awareness of this anatomical structure and routine CTV when there is extension of skull fracture line to the major dural sinuses is important for appropriate diagnosis.

Glycosylation, hypogammaglobulinemia, and resistance to viral infections.

MA Sadat, S Moir, TW Chun. N Engl J Med. 2014;370(17):1615–1625 The goal of this study was to elucidate viral resistance despite immunodeficiency in a rare congenital disorder of glycosylation type IIb. The study subjects were 2 siblings presenting with multiple neurologic complications and a paradoxical immunologic phenotype characterized by severe hypogammaglobulinemia but limited clinical evidence of recurrent severe infections. An 11-year-old …

Glycosylation, Hypogammaglobulinemia, and Resistance to Viral Infections

Genetic defects in MOGS, the gene encoding mannosyl-oligosaccharide glucosidase (the first enzyme in the processing pathway of N-linked oligosaccharide), cause the rare congenital disorder of glycosylation type IIb (CDG-IIb), also known as MOGS-CDG. MOGS is expressed in the endoplasmic reticulum and is involved in the trimming of N-glycans. We evaluated two siblings with CDG-IIb who presented with multiple neurologic complications and a paradoxical immunologic phenotype characterized by severe hypogammaglobulinemia but limited clinical evidence of an infectious diathesis. A shortened immunoglobulin half-life was determined to be the mechanism underlying the hypogammaglobulinemia. Impaired viral replication and cellular entry may explain a decreased susceptibility to infections.

Lymphomatoid granulomatosis presenting as tinnitus in a patient with acquired immunodeficiency syndrome

Introduction: Puzzling neurologic symptoms in an immunosuppressed patient presents the clinician with a broad and challenging differential diagnosis. Multiple neurological complications in human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS)-infected individuals have been reported, the most common being cognitive dysfunction, infections, and malignancies. In patients with advanced immunosuppression any neurological symptom should be taken seriously. We report a case of Epstein–Barr virus (EBV) related lymphomatoid granulomatosis presenting in a patient with AIDS initially as tinnitus. Case Report: A 42-year-old female was presented to her physician complaining of tinnitus. Unbeknownst to her physician, she had been diagnosed with human immunodeficiency virus (HIV) 14 years prior. Her tinnitus led her to undergo a workup in outpatient clinic. However, her neurological symptoms gradually progressed to include hearing loss and diplopia. She was admitted to another hospital and underwent an extensive array of testing. Laboratory testing indicated that her HIV had progressed to AIDS. Neurological imaging revealed a brainstem lesion. She was transferred to our hospital when the brainstem lesion was deemed inaccessible by neurosurgery. Several small pulmonary nodules had been noted on computed tomography scan of her chest. Surgical biopsy with pathology and flow cytometry of a lung nodule showed EBV-related lymphomatoid granulomatosis. Soon after, a unifying diagnosis between her lung nodules and a central nervous system disease was made as flow cytometry of her cerebrospinal fluid showed an identical aberrant B cell population consistent with lymphomatoid granulomatosis with transformation to diffuse large B cell lymphoma. Unfortunately, patient's brainstem lesions progressed and patient died after a few weeks in the hospital. Conclusion: Epstein–Barr virus related lymphomatoid granulomatosis is a rare disease that can be the cause of unexplained neurological symptoms in immunocompromised individuals. We report a challenging case in which the diagnosis was only considered after lung biopsy of relatively asymptomatic pulmonary nodules.

Chapter 10 - Molecular and neurologic responses to chronic alcohol use

This chapter provides an overview of current knowledge on the molecular and clinical aspects of chronic alcohol effects on the central nervous system. This drug is almost ubiquitous, widely enjoyed socially, but produces a diverse spectrum of neurologic disease when abused. Acutely, alcohol interacts predominantly with γ-aminobutyric acid-A (GABA-A) and N-methyl-d-aspartate (NMDA) receptors, but triggers diverse signaling events within well-defined neural pathways. These events result in adaptive changes in gene expression that ultimately produce two major states: addiction and toxicity. Epigenetic modifications of chromatin could lead to long-lived or even transgenerational changes in gene expression, thus producing aspects of the heritability of alcohol use disorders (AUD) and long-term behaviors such as recidivism. The diverse clinical syndromes produced by chronic alcohol actions in the central nervous system reflect the molecular pathology and predominantly involve aspects of tolerance/withdrawal, selective vulnerability (manifest as central pontine myelinolysis, Marchiafava-Bignami disease), and additional environmental factors (e.g., thiamine deficiency in Wernicke-Korsakoff's syndrome). Additionally, deleterious aspects of chronic alcohol on signaling, synaptic transmission, and cell toxicity lead to primary alcoholic dementia. Genetically determined aspects of myelin structure and alcohol actions on myelin gene expression may be a prominent molecular mechanism resulting in a predisposition to, or causation of, AUD and multiple other neurologic complications of chronic alcohol. The dramatic progress made in understanding molecular actions of alcohol holds great promise for our eventual treatment or prevention of AUD and neurologic complications resulting from chronic alcohol abuse.

Delayed Recurrent Stroke in a Young Patient with Acute Posterior Multifocal Placoid Pigment Epitheliopathy

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is a chorioretinal disease that causes acute binocular visual disturbance with characteristic funduscopic lesions at the level of the retinal pigment epithelium. APMPPE has been associated with multiple neurologic complications, including cerebrovascular diseases. We report a 15-year-old patient who had bilateral APMPPE, which was successfully treated with corticosteroids. One year later he presented with transient dysarthria and right hemiparesis. Brain magnetic resonance imaging (MRI) showed bilateral ischemic lesions in both lenticular nuclei and corona radiata. Brain MRI performed 3 months later revealed a new asymptomatic ischemic lesion. Cerebral angiography showed diffuse multifocal segmental vessel narrowing. The cerebrospinal fluid showed mononuclear pleocytosis in keeping with vasculitis. We started corticosteroid treatment, which lasted 10 months. Currently, after 2 years of clinical and neuroradiologic follow-up, the patient is asymptomatic and shows no worsening of the cerebrovascular lesions.

Effect of rebleeding on the course and incidence of vasospasm after subarachnoid hemorrhage

Rebleeding of an aneurysm is a leading cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Whereas numerous studies have demonstrated the risk factors associated with rebleeding, few data on complications of rebleeding, including its effect on the development of delayed cerebral ischemia (DCI), are available. A nested case-control study was performed on patients with rebleeding and control subjects matched for modified Fisher scale, Hunt-Hess grade, age, and sex previously entered into a prospective database. Rebleeding was defined as new hemorrhage apparent on repeat CT with or without new symptoms. Incidence and time course of DCI and hospital complications were compared. A secondary analysis of DCI and hospital complications was also performed on subjects surviving to postbleed day 7. We identified 120 patients with rebleeding and 359 control subjects from 1996 to 2011. The rebleeding rate was 8.6%. In both the primary and secondary analyses, there was no difference in the incidence of DCI or its time course (29% vs. 27%, p = 0.6; 7 ± 5 vs. 7 ± 6 days, p = 0.9 for primary analysis; 39% vs. 31%, p = 0.1, 7 ± 5 vs. 7 ± 6 days, p = 0.6 for the secondary analysis). In a multivariate logistic regression model, rebleeding was associated with the complications of hyponatremia, respiratory failure, and hydrocephalus. Patients with rebleeding had higher rates of mortality, brain death, and poor outcomes. Rebleeding after SAH is associated with multiple medical and neurologic complications, resulting in higher morbidity and mortality, but is not associated with change of incidence or timing of DCI.

Safety of Chiropractic Interventions

Systematic review of reported adverse events. To evaluate the tolerability and safety of chiropractic procedures. Despite the increasing popularity of chiropractic, there are few properly designed prospective controlled trials, and there is a disproportionate lack of evaluation of its safety profile. The literature reports multiple neurologic complications of spinal manipulation, some of which are clinically relevant and even life threatening. We performed an electronic search in 2 databases: Pubmed and the Cochrane Library for the years 1966 to 2007. All articles that reported adverse reactions associated with chiropractic were included irrespective of type of design. The outcome measures were the type of adverse events associated or attributed to chiropractic interventions and their frequency. A total of 376 potential relevant articles were identified, 330 of which were discarded after abstract or complete article analysis. The search identified 46 articles that included data concerning adverse events: 1 randomized controlled trial, 2 case-control studies, 7 prospective studies, 12 surveys, 3 retrospective studies, and 115 case reports. Most of the adverse events reported were benign and transitory, however, there are reports of complications that were life threatening, such as arterial dissection, myelopathy, vertebral disc extrusion, and epidural hematoma. The frequency of adverse events varied between 33% and 60.9%, and the frequency of serious adverse events varied between 5 strokes/100,000 manipulations to 1.46 serious adverse events/10,000,000 manipulations and 2.68 deaths/10,000,000 manipulations. There is no robust data concerning the incidence or prevalence of adverse reactions after chiropractic. Further investigations are urgently needed to assess definite conclusions regarding this issue.

Polyneuropathy and Cerebral Infarction Complicating Scrub Typhus

We describe a 64-year-old man with scrub typhus who presented with both polyneuropathy and cerebral infarction. A eurological examination revealed a confused mental state, stiff neck, hearing impairment, symmetric weakness, sensory loss, and ataxia. Electrophysiologic studies showed demyelinating sensorimotor polyneuropathy and sensorineural hearing loss. Brain magnetic resonance imaging showed multiple infarctions. Brain involvement or polyneuropathy associated with scrub typhus has been rarely reported, and the pathogenic mechanism underlying the multiple neurological complications remains to be elucidated.

The protean neurologic manifestations of varicella-zoster virus infection.

Multiple neurologic complications may follow the reactivation of varicella-zoster virus (VZV), including herpes zoster (also known as zoster or shingles), postherpetic neuralgia, vasculopathy, myelitis, necrotizing retinitis, and zoster sine herpete (pain without rash). These conditions can be difficult to recognize, especially as several can occur without rash.

Neuroimaging in Drug and Substance Abuse Part I

Multiple neurological complications of cocaine abuse have been described including both ischemic and hemorrhagic cerebrovascular events, atrophy in the case of chronic abuse, and an increase in incidence of congenital malformations in the setting of maternal use. The abuse of cannabis may cause a number of neurovascular changes that, in turn, may result in ischemic events, however, a direct connection between these has not been fully established. The use of MDMA (ecstasy), a popular recreational drug, has been related to ischemic and hemorrhagic cerebrovascular events, as well as atrophy. Neuroimaging studies are vital in the assessment of the extent of neurologic damage in these patients.