Alice in Wonderland syndrome as aura of migraine

Alice in Wonderland syndrome (AIWS), named for Lewis Carroll’s titular character, is a disorder characterized by transient episodes of visual hallucinations and perceptual distortions, during which objects or body parts are perceived as altered in various ways (metamorphopsia), including enlargement (macropsia) or reduction (micropsia) in the perceived size of a form. Migraine aura is a transient neurological symptom that most commonly involves the visual fields and occurs before the headache phase. Aura symptoms include the perception of flashing lights that begin in the center of vision and expand in jagged patterns out into the periphery. Symptoms may be somatosensory, such as numbness and tingling in the lips or fingers. They may also involve a profound alteration of the perception of space and time (the “Alice in Wonderland” syndrome). In this article, we present a child had Alice in Wonderland syndrome as aura of migraine.     

Alice in Wonderland syndrome: a lesion mapping study

Neurological Sciences - Alice in Wonderland syndrome (AIWS) is a rare neurological disorder, characterized by an erroneous perception of the body schema or surrounding space. It may be caused by a...     

Abnormal magnetic resonance imaging in a child with Alice in Wonderland syndrome following Epstein-Barr virus infection

Characteristic pathologic changes of cranial computed tomography (CT) and magnetic resonance imaging (MRI) have never been reported in "Alice in Wonderland" syndrome (AIWS) caused by Epstein-Barr (EB) virus infection. We present here a 10-year-old girl with AIWS with an abnormal MR finding. During the course of serologically confirmed EB virus encephalopathy, she had distortion of the body image, visual hallucinations and depersonalization characteristic of AIWS. MRI demonstrated transient T2 prolongation and swelling of the cerebral cortex, especially at the bilateral temporal lobes, bilateral cingulate gyrus, right upper frontal gyrus, bilateral caudate nucleus, and bilateral putamen, whereas CT showed no abnormalities. Transient MRI lesions were occasionally reported in patients with EB virus encephalopathy/encephalitis who presented visual illusions and psychotic reactions, although the diagnosis of AIWS was not described. We consider that any patient with symptoms of AIWS should have MRI because the abnormal MRI findings may disappear in a short period.     

Serum antibodies to Epstein-Barr virus in patients with major depressive disorder

To determine whether major depressive disorder might be associated with serologic evidence for a chronic active Epstein-Barr virus infection, viral-specific antibodies were measured in two separate groups of depressed patients (N=43) and in 46 appropriately matched healthy volunteers. No evidence that depression affects cellular immunity to the point that a persistent Epstein-Barr virus carrier state becomes activated was found. There was also no evidence that depression results from an unrecognized chronic active Epstein-Barr virus infection. The authors conclude that the routine clinical determination of expensive commercial Epstein-Barr virus antibody profiles is not indicated in most patients with major depressive disorder in the absence of other signs of chronic active Epstein-Barr viral infection.     

Temporal–occipital glioblastoma presenting with Alice in Wonderland Syndrome in a patient with a long-time history of migraine without aura

ABSTRACT

Alice in Wonderland Syndrome (AIWS) is a rare perceptual disorder characterized by an erroneous perception of the body or the surrounding space. AIWS may be caused by different pathologies, ranging from infections to migraine. We present the case of a 54-year-old man, with a long-time history of migraine without aura, diagnosed with AIWS due to a glioblastoma located in the left temporal–occipital junction. To date, this is the first case of AIWS caused by glioblastoma. This case suggests that to exclude aura-mimic phenomena, a careful diagnostic workup should always be performed even in patients with a long-time history of migraine.     

The Alice in Worderland Syndrome

ABSTRACT

The Alice in Wonderland Syndrome (AWS) was first described more than 60 years ago by Lippman. It refers to episodes during which an individual may variously experience (as did Alice during her time in Wonderland) somatic, visuo-perceptual and/or visuo-spatial hallucinations, as well as feelings of depersonalisation, derealisation and distorted sense of time. Although the prevalence of AWS is unknown, indirect evidence from both retrospective and prospective studies suggests that it is a rare disorder. This paper describes the case of Zoe, a right-handed, native English speaker who was age 45 years when she experienced an episode of AWS. On neuropsychological assessment, Zoe demonstrated notable impairment of attention, learning and recall (particularly for visuo-spatial information) as well as executive dysfunction (viz., impairment of planning, cognitive flexibility and abstraction), consistent with fronto-temporal dysfunction. Detailed profiles of neuropsychological impairment in the context of AWS have not previously been reported, and it is unclear if such impairment is, indeed, a central and characteristic feature of AWS.     

The Alice in Wonderland syndrome: an unusual aura in migraine

IntroductionThe Alice in Wonderland syndrome consists in a perceptual distortion of one's body size and shape. It is rarely encountered in adults, where it is mainly associated with migraine with aura and epilepsy.Case reportA 37-year-old woman had had a migraine without aura since puberty. In the months following a parturition, she experienced several epidodes of unusual auras preceding typical migrainous headache. The aura lasted about 30 min and consisted in the feeling of lengthening of the trunk and of the four limbs, associated with a sensation of well-being.Discussion and conclusionEpileptologic and experimental data suggest that the Alice in Wonderland syndrome is associated with a transient dysfunction of associative somatosensory areas in the parietal cortex.     

Lyme neuroborreliosis presenting as Alice in Wonderland syndrome

We describe a 7-year-old boy with Alice in Wonderland syndrome associated with Lyme disease. He presented with metamorphopsia and auditory hallucinations in the absence of previous tick bites or other signs of Lyme disease. The boy never developed clinical seizures, and electroencephalograms during these spells indicated no epileptic activity. There was no history of migraine. Cranial magnetic resonance imaging produced normal results. Lyme serology tested positive in both serum and cerebrospinal fluid. He was treated with intravenous ceftriaxone for 3 weeks, with complete resolution of signs. This case report is the first, to our knowledge, of neuroborreliosis presenting as Alice in Wonderland syndrome with complete resolution of findings after intravenous antibiotic treatment.     

Alice in Wonderland syndrome: a novel neurological presentation of Zika virus infection

Zika virus (ZIKV) is a flavivirus endemic in Africa and Southern Asian countries, which has recently emerged in unprecedented epidemic proportions around the world. Although ZIKV infection is often asymptomatic or distinguished by non-specific influenza-like symptoms, an increase in its pathogenicity and biological behavior has been the hallmark of the current pandemic. Increasing evidence suggests that neurotropic strains of ZIKV have evolved from less pathogenic strains of the virus. Neurological manifestations of ZIKV infection include a spectrum of congenital and non-congenital clinical entities, however visual somatosensory perceptual disorders have not been recorded to date. Herein, we report a case of a 15-year-old female who presented with a constellation of perceptual symptoms (metamorphopsia, telopsia, and pelopsia) following acute ZIKV infection. Although such symptoms may have originated from direct viral injury, a post-ZIKV autoimmune reaction to previously unexposed neuronal surface antigens or through molecular mimicry cannot be excluded. The development of Alice in Wonderland syndrome in our patient highlights the ever-increasing expanding spectrum of neurological symptoms associated to ZIKV infection.     

Abnormal visual evoked potentials in children with "Alice in Wonderland" syndrome due to infectious mononucleosis

Visual illusions characterized by distortion of form, size, reciprocal position of objects, movement, or color, labeled as "Alice in Wonderland" syndrome, were discussed in children with infectious mononucleosis, as well as in other clinical conditions, such as migraine, epilepsy, use of certain hallucinogenic drugs, etc. The purpose of our study was to investigate for the first time visual evoked potential results in children with "Alice in Wonderland" syndrome associated with infectious mononucleosis. Five children with "Alice in Wonderland" syndrome associated with infectious mononucleosis underwent visual evoked potential studies during and after their clinical symptoms. Visual evoked potential results during the disease demonstrated statistically significant high amplitudes of P100-N145 in all children compared to the control group. A few weeks later, repeated studies after the resolution of the complaints were normal. Since the same findings can be observed in patients with migraine, we postulate that a common pathophysiologic underlying abnormality, which can cause transient focal decreased cerebral perfusion, could be involved in the disease process of these two conditions.     

Adenovirus type 2 encephalitis and concurrent Epstein-Barr virus infection in an adult man

A 30-year-old bisexual male prisoner with a history of intravenous drug abuse manifested encephalitis. Adenovirus type 2 was isolated from brain tissue obtained by a biopsy and there was a concurrent fourfold rise in the antibody titer. In addition, an initial negative result from a slide test for infectious mononucleosis heterophil antibodies (Monospot) test converted to positive and there was an increase in the IgG antibody titer to Epstein-Barr virus (EBV) viral capsid antigen. Although he was anergic to skin test antigens, T-cell subsets and lymphocyte transformation study results were normal. This case demonstrated a rare adenovirus encephalitis with a simultaneous EBV infection in a patient at risk for acquired immunodeficiency syndrome, who had minimal evidence of T-cell deficiency.     

Correlation between cytomegalovirus infection and IgM anti-MAG/SGPG antibody–associated neuropathy

IgM anti–myelin-associated glycoprotein (anti-MAG)/sulfated glucuronyl paragloboside (SGPG) antibody is found in some patients with chronic polyneuropathy (CP). An antigen-driven process is considered to induce this autoantibody, but the agent has yet to be identified. It has been reported that sera from cytomegalofvirus (CMV)-infected patients contained anti-SGPG antibody. To clarify the mechanism of the production of the anti-MAG/SGPG antibody, we investigated CMV DNA in sera from 26 patients with IgM anti-MAG/SGPG antibody–positive CP. Twenty-three (88%) had CMV DNA. The positive frequency was significantly higher than the freqencies in sera from patients with IgM anti-MAG/SGPG–negative CP, the other disease controls, and the normal control subjects. There were no statistical differences in the frequencies of Epstein-Barr virus DNA between anti-MAG/SGPG–positive and anti-MAG/SGPG–negative CP and between anti-MAG/SGPG–positive CP and each disease control. Moreover, no herpes simplex virus 1 DNA was detected in the sera from patients with anti-MAG/SGPG–positive CP. The strong correlation of anti-MAG/SGPG–positive CP with the presence of serum CMV DNA suggests that CMV infection induces the IgM anti-MAG/SGPG antibody.     

Pediatric Epstein-Barr virus-associated encephalitis: 10-year review

Many neurologic manifestations of Epstein-Barr virus (EBV) infection have been documented, including encephalitis, aseptic meningitis, transverse myelitis, and Guillain-Barré syndrome. These manifestations can occur alone or coincidentally with the clinical picture of infectious mononucleosis. Since 1994, The Hospital for Sick Children has maintained a prospective registry of all children admitted with acute encephalitis. This report summarizes all cases of Epstein-Barr virus-associated encephalitis compiled from 1994 to 2003. Twenty-one (6%) of 216 children, median age 13 years (range 3-17 years), in the Encephalitis Registry were identified as having evidence of Epstein-Barr virus infection. This evidence consisted of convincing Epstein-Barr virus serology and/or positive cerebrospinal fluid polymerase chain reaction (PCR). One patient had symptoms of classic infectious mononucleosis; all others had a nonspecific prodrome, including fever (n = 17; 81%) and headache (n = 14; 66%). Slightly less than half (n = 10; 48%) had seizures and often had electroencephalograms showing a slow background (n = 12; 57%). Many demonstrated cerebrospinal fluid pleocytosis (n = 17; 81%), and 71% (n = 15) had abnormal magnetic resonance imaging findings. Two patients died, 2 suffered mild deficits, and 16 were neurologically normal at follow-up. Most patients with Epstein-Barr virus encephalitis do not show typical symptoms of infectious mononucleosis. Establishing a diagnosis of Epstein-Barr virus encephalitis can be difficult, and, consequently, a combination of serologic and molecular techniques should be used when investigating a child with acute encephalitis. Most children make full recoveries, but residual neurologic sequelae and even death can and do occur.     

Guillain-Barré Syndrome Associated with Epstein-Barr Virus in a Cytomegalovirus-negative Patient

Epstein-Barr virus and cytomegalovirus have both been associated with Guillain-Barré syndrome after antibody investigations in several patients. In the teenage female patient in this present report, Guillain-Barré syndrome following infectious mononucleosis was associated with sero-conversion against Epstein-Barr virus but not cytomegalovirus. The findings are consistent with the hypothesis that Epstein-Barr virus might be an etiological agent for the Guillain-Barré syndrome and that infection with cytomegalovirus is not a requisite for the syndrome.     

Acute peripheral facial palsy: CSF findings and etiology

CSF and serum were examined in acute and convalescence phase from 56 patients with acute idiopathic peripheral facial palsy. CSF protein analysis, viral and borrelia serology were performed. Borrelia infection was found in 9/56 cases and was often associated with inflammatory CSF findings. One patient each had serological evidence for a recent or ongoing infection with herpes simplex, varicella zoster, adeno, influenza B, echo and Epstein-Barr virus, but none had specific intrathecal antibody synthesis; 11 patients had a serological pattern compatible with a reactivated Epstein-Barr virus infection. Eleven patients displayed mononuclear CSF pleocytosis. Four of them had a borrelia infection. A disturbed blood-brain barrier was observed in 19 patients. Intrathecal immunoglobulin synthesis as indicated by elevated IgM-indices was found in 16 patients and by IgG indices in three. Nine patients had oligoclonal IgG bands in serum and CSF, three exclusively in CSF. It is concluded that patients with facial palsy often have inflammatory CSF findings, indicating a generalised central nervous system affection, and not only a mononeuritis. The importance of viral infections in the pathogenesis is still obscure. Borrelia is the most common infectious cause of facial palsy.     

Absence of Epstein-Barr virus RNA in multiple sclerosis as assessed by in situ hybridisation.

Epidemiological and serological evidence has suggested a role for Epstein-Barr virus infection in the aetiology of multiple sclerosis. Epstein-Barr virus-specific RNA was looked for in the brains of 10 patients with multiple sclerosis by in situ hybridisation. A total of 21 plaques was examined. In all of these preservation of RNA was shown by hybridisation of control probes to mitochondrial rRNA but no signal was detected with the Epstein-Barr virus probes. It is unlikely that persistent or latent Epstein-Barr virus infection of the CNS occurs in multiple sclerosis, although present findings do not exclude a role for Epstein-Barr virus in the initiation of this disorder.     

Persistent preceding focal neurologic deficits in children with chronic Epstein-Barr virus encephalitis

Epstein-Barr virus encephalitis is a self-limiting disease with few sequelae. Persistence of neurologic deficits prior to and after the acute illness has yet to be described in children. We describe five children with persistent cognitive and focal neurologic deficits due to chronic Epstein-Barr virus encephalitis with various T2-weighted magnetic resonance imaging abnormalities. Clinical features were a 9-year-old boy with aphasia and apraxia, an 11-year-old girl with impulsivity and inappropriate behavior, a 17-year-old boy with deterioration of cognitive skills and judgment, a 5-year-old boy with complex-partial seizures, and a 6-year-old girl with obsessive-compulsive behavior. All patients had elevated serum Epstein-Barr virus titers for acute infection, with cerebrospinal fluid polymerase chain reaction positive for Epstein-Barr virus in four patients. Three children were treated with methylprednisolone with minimal improvement without changes on magnetic resonance imaging. Epstein-Barr virus encephalitis can present with chronic and insidious neurologic symptoms and should be considered in the differential diagnosis of children with acute or chronic neurologic illness of unknown etiology.     

Mollaret's meningitis associated with acute Epstein-Barr virus mononucleosis

A 19-year-old man developed recurrent aseptic meningitis (Mollaret's meningitis) during the course of acute Epstein-Barr virus infectious mononucleosis. Serum contained heterophil antibody and Epstein-Barr virus-specific antibodies characteristic of acute infection. Seven brief episodes of aseptic meningitis were documented over the following one-year period, in each case with a polymorphonuclear pleocytosis in the cerebrospinal fluid. Acute infection with Epstein-Barr virus, or subsequent reactivation of virus, may account for some cases of Mollaret's meningitis.     

Autoantibodies in postinfectious acute cerebellar ataxia

The authors found serum immunoglobulin M (IgM) autoantibody in a patient with typical acute cerebellar ataxia (ACA) and identified the antigen molecule as triosephosphate isomerase (TPI). TPI antigenicity to the patient's antibody was the highest in the cerebellar tissue. Eight of 23 patients with ACA had increased IgM anti-TPI antibody titers vs those of healthy controls. Preceding Epstein-Barr virus infection was confirmed serologically in all 8 patients. Anti-TPI antibody decreased with clinical improvement.