Isolated Memory Loss in Anti-NMDAR Encephalitis

Background and ObjectivesTo report a case of anti-NMDAR encephalitis presenting with isolated memory dysfunction.MethodsA 29-year-old woman was admitted to the Neurology Department referring memory impairment with a subacute onset. The initial assessment included EEG, neuropsychological tests, and brain MRI. Serum and CSF samples were collected for immunologic studies. The diagnostic evaluation was completed with a total body PET scan.ResultsPatient's neurologic examination was unremarkable apart from an episodic memory deficit, confirmed by neuropsychological examination. The EEG revealed epileptiform discharges in the temporal lobes, whereas brain MRI showed bilateral temporal lobes hyperintense lesions on fluid-attenuated inversion recovery images and T2-weighted images. NMDAR-IgG was detected in the patient's serum and CSF by cell-based assay confirming the diagnosis of definite anti-NMDAR encephalitis. The total body PET showed only a slight hypometabolism in the right temporal cortex and in the cerebellar hemispheres. After a course of IV immunoglobulin and corticosteroid therapy, a marked improvement of the memory deficit was observed.DiscussionThis case shows that anti-NMDAR encephalitis can present with isolated memory loss. Neural antibody testing in these patients could play a pivotal role in early diagnosis and prompt treatment.

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Antibody-associated CNS syndromes without signs of inflammation in the elderly

Neurology ◽

10.1212/wnl.0000000000004541 ◽

2017 ◽

Vol 89 (14) ◽

pp. 1471-1475 ◽

Cited By ~ 34

Author(s):

Domingo Escudero ◽

Mar Guasp ◽

Helena Ariño ◽

Carles Gaig ◽

Eugenia Martínez-Hernández ◽

...

Keyword(s):

Neurodegenerative Disorder ◽

Brain Mri ◽

Clinical Manifestations ◽

Memory Loss ◽

Autoimmune Encephalitis ◽

Surface Antigens ◽

Clinical Analysis ◽

Correct Identification ◽

Cognitive Deterioration ◽

Antibody Testing

Objective:To report the CNS syndromes of patients ≥60 years of age with antibodies against neuronal surface antigens but no evidence of brain MRI and CSF inflammatory changes.Methods:This was a retrospective clinical analysis of patients with antibodies against neuronal surface antigens who fulfilled 3 criteria: age ≥60 years, no inflammatory abnormalities in brain MRI, and no CSF pleocytosis. Antibodies were determined with reported techniques.Results:Among 155 patients ≥60 years of age with neurologic syndromes related to antibodies against neuronal surface antigens, 35 (22.6%) fulfilled the indicated criteria. The median age of these 35 patients was 68 years (range 60–88 years). Clinical manifestations included faciobrachial dystonic seizures (FBDS) in 11 of 35 (31.4%) patients, all with LGI1 antibodies; a combination of gait instability, brainstem dysfunction, and sleep disorder associated with IgLON5 antibodies in 10 (28.6%); acute confusion, memory loss, and behavioral changes suggesting autoimmune encephalitis (AE) in 9 (25.7%; 2 patients with AMPAR, 2 with NMDAR, 2 with GABAbR, 2 with LGI1, and 1 with CASPR2 antibodies); and rapidly progressive cognitive deterioration in 5 (14.3%; 3 patients with IgLON5 antibodies, 1 with chorea; 1 with DPPX antibody–associated cerebellar ataxia and arm rigidity; and 1 with CASPR2 antibodies).Conclusions:In patients ≥60 years of age, the correct identification of characteristic CNS syndromes (FBDS, anti-IgLON5 syndrome, AE) should prompt antibody testing even without evidence of inflammation in MRI and CSF studies. Up to 15% of the patients developed rapidly progressive cognitive deterioration, which further complicated the differential diagnosis with a neurodegenerative disorder.

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A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats

Synapse ◽

10.1002/syn.21832 ◽

2015 ◽

Vol 69 (9) ◽

pp. 421-433 ◽

Cited By ~ 41

Author(s):

Samuel Treviño ◽

Patrícia Aguilar-Alonso ◽

Jose Angel Flores Hernandez ◽

Eduardo Brambila ◽

Jorge Guevara ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Temporal Cortex ◽

Memory Loss ◽

Calorie Diet ◽

And Oxidative Stress ◽

High Calorie Diet ◽

High Calorie

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Case of early-onset Alzheimer’s disease with atypical manifestation

General Psychiatry ◽

10.1136/gpsych-2020-100283 ◽

2021 ◽

Vol 34 (1) ◽

pp. e100283

Author(s):

Lin Zhu ◽

Limin Sun ◽

Lin Sun ◽

Shifu Xiao

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Clinical Manifestation ◽

Early Onset ◽

Short Term Memory ◽

Brain Mri ◽

Memory Loss ◽

Amyloid Β ◽

Amyloid Β Protein ◽

Fluent Aphasia

Short-term memory decline is the typical clinical manifestation of Alzheimer’s disease (AD). However, early-onset AD usually has atypical symptoms and may get misdiagnosed. In the present case study, we reported a patient who experienced symptoms of memory loss with progressive non-fluent aphasia accompanied by gradual social withdrawal. He did not meet the diagnostic criteria of AD based on the clinical manifestation and brain MRI. However, his cerebrospinal fluid examination showed a decreased level of beta-amyloid 42, and increased total tau and phosphorylated tau. Massive amyloid β-protein deposition by 11C-Pittsburgh positron emission tomography confirmed the diagnosis of frontal variant AD. This case indicated that early-onset AD may have progressive non-fluent aphasia as the core manifestation. The combination of individual and precision diagnosis would be beneficial for similar cases.

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Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Recurrent and Migrating Focal Cortical Encephalitis

Child Neurology Open ◽

10.1177/2329048x20966172 ◽

2020 ◽

Vol 7 ◽

pp. 2329048X2096617

Author(s):

Xinran Maria Xiang ◽

Rachel Evans ◽

Jesus Lovera ◽

Rashmi Rao

Keyword(s):

Brain Mri ◽

Occipital Cortex ◽

Myelin Oligodendrocyte Glycoprotein ◽

New Right ◽

High Dose ◽

Antibody Testing ◽

Leptomeningeal Enhancement ◽

The Right ◽

Work Up ◽

New Onset

Although pediatric myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease is increasingly well-recognized, its full clinical spectrum is still being defined. Cortical encephalitis is emerging as a distinct clinico-radiologic syndrome of adult MOG antibody-associated disease. We describe a 12-year-old girl who presented with new onset seizures and left-sided hemiparesis. Brain MRI showed edema of the right temporal-parietal-occipital cortex with associated focal leptomeningeal enhancement. Patient received high-dose corticosteroids and 21 days of acyclovir despite negative infectious work-up due to the focal nature of encephalitis. Patient remained seizure-free for 20 months before presenting with new right hemiclonic seizures with right-sided hemiparesis and edema of the left temporal-parietal cortex with associated leptomeningeal enhancement. Patient’s MOG antibody titer was 1:40. She completed high-dose corticosteroids and intravenous immunoglobulin. Our patient highlights the importance of MOG antibody testing in pediatric focal cortical encephalitis to avoid unnecessary anti-viral agents and provide more appropriate immunotherapy and a more informed prognosis.

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Pavlov, Penfield, and the physiology of the mind

Neurology ◽

10.1212/wnl.0000000000007145 ◽

2019 ◽

Vol 92 (12) ◽

pp. 575-578 ◽

Cited By ~ 1

Author(s):

Richard Leblanc

Keyword(s):

Conditioned Reflex ◽

Functional Integration ◽

Temporal Cortex ◽

Spoken Language ◽

Conditioned Reflexes ◽

Temporal Lobes ◽

Past Experiences ◽

The Mind ◽

The Brain ◽

Stimulation Of

Wilder Penfield's contributions to the structure–function relationships of the brain are well-known. Less well-known is the influence that Ivan Pavlov and the conditioned reflex had on Penfield's understanding of epileptogenesis, and on his concept of the acquisition of memories, language, and perception—what Penfield referred to as the physiology of the mind. Penfield invoked conditioned reflexes to explain responses to electrocortical stimulation of the temporal lobes that encompass memory, perception, and affect. Penfield referred to these responses as experiential phenomena since he considered that they constituted a record of past experiences. Penfield also invoked the conditioned reflex to explain the acquisition of the interpretive aspects of written and spoken language in the dominant temporal cortex. This article describes and discusses these neglected aspects of Penfield's work, and how they contributed to a broader understanding of the functional integration of the temporal cortex and the limbic system.

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The diffuse involvement of anti-N-methyl-D-aspartate receptor encephalitis in brain: a case report

BMC Neurology ◽

10.1186/s12883-019-1456-6 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 1

Author(s):

Yun Jiang ◽

Jianpeng Ma ◽

Tao Gong ◽

Hongjun Hao ◽

Haibo Chen

Keyword(s):

Basal Ganglia ◽

Brain Mri ◽

Clinical Manifestations ◽

Autoimmune Encephalitis ◽

Ovarian Teratoma ◽

Mass Effects ◽

Glucose Levels ◽

Aspartate Receptor ◽

Nmdar Encephalitis ◽

Case Presentations

Abstract Background Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe and most common autoimmune encephalitis in patients under 40 years old. Anti-NMDAR encephalitis has various clinical and neuroimaging findings. Here we report a special case of an anti-NMDAR encephalitis who had diffuse lesions in bilateral hemispheres with mild mass effects in left basal ganglia area. Case presentations A 28-year-old female anti-NMDAR encephalitis patient mainly presented with headache and fever. Brain magnetic resonance image (MRI) showed slightly contrasted diffuse lesions, involving the left temporal and frontal lobes, left basal ganglia area and splenium of corpus callosum, as well as the right frontal lobe, with mild edema surrounded in the left basal ganglia area. Cerebrospinal fluid (CSF) revealed a moderate pleocytosis with normal protein and glucose levels. Anti-NMDAR antibodies were identified in CSF. Transvaginal ovarian ultrasound did not reveal an ovarian teratoma. The patient was treated with immunoglobulin and steroid, and had a good recovery. Conclusions Anti-NMDAR encephalitis has no special clinical manifestations and brain MRI is highly variable, which could be unremarkable or abnormal involving white and grey matters. The extensive lesions in frontal and temporal lobes, and basal ganglia area, with mild mass effects, have not been described previously. Recognition of various changes in brain MRI will enable the early detection of anti-NMDAR antibody and then effective treatments.

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Partly reversible central auditory dysfunction induced by cerebral vasospasm after subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/2013.7.jns13674 ◽

2013 ◽

Vol 119 (5) ◽

pp. 1125-1128 ◽

Cited By ~ 5

Author(s):

Ester Ponzetto ◽

Marco Vinetti ◽

Cécile Grandin ◽

Thierry Duprez ◽

Vincent van Pesch ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Auditory Evoked Potentials ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Rare Complication ◽

Brain Mri ◽

Temporal Cortex ◽

Intraarterial Infusion ◽

Auditory Dysfunction ◽

The Right

The authors describe a rare case of central auditory dysfunction induced by cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). A 55-year-old woman who was admitted after aneurysmal SAH developed cerebral vasospasm on Day 3 affecting mainly the right middle cerebral artery (MCA) and partly the left MCA. The vasospasm became refractory to conventional therapy and was ultimately improved by intraarterial infusion of nimodipine in the right MCA and angioplasty. Severe auditory dysfunction was apparent from Day 10 as the patient was not reactive to speech or environmental sounds. Brain MRI on Day 17 demonstrated infarcted areas mainly in the right hippocampus, medial occipital lobe, and thalamus. The patient underwent further examination using audiometry, speech testing, auditory evoked potentials, functional MRI, and cerebral PET. The initial diagnosis was extended nonverbal agnosia and total pure word deafness. The central auditory dysfunction improved over 6 months, with persisting hyperacusis, tinnitus, and amusia. Central auditory dysfunction is a rare complication after SAH. While cortical deafness may be associated with bilateral lesions of the temporal cortex, partly reversible central auditory dysfunction was observed in this patient after prominently unilateral right temporal lesions. The role of the interthalamic connections can be discussed, as well as the possibility that a less severe vasospasm on the left MCA could have transiently impaired the left thalamocortical auditory pathways.

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Persistent Autobiographical Amnesia: A Case Report

Behavioural Neurology ◽

10.1155/2007/534043 ◽

2007 ◽

Vol 18 (1) ◽

pp. 13-17 ◽

Cited By ~ 7

Author(s):

C. Repetto ◽

R. Manenti ◽

V. Sansone ◽

M. Cotelli ◽

D. Perani ◽

...

Keyword(s):

Brain Mri ◽

Motor Impairment ◽

Acute Onset ◽

Memory Deficit ◽

Learning Abilities ◽

Arterial Blood ◽

Retrograde Memory ◽

Global Amnesia ◽

One Year ◽

The Right

We describe a 47-year-old man who referred to the Emergency Department for sudden global amnesia and left mild motor impairment in the setting of increased arterial blood pressure. The acute episode resolved within 24 hours. Despite general recovery and the apparent transitory nature of the event, a persistent selective impairment in recollecting events from some specific topics of his personal life became apparent. Complete neuropsychological tests one week after the acute onset and 2 months later demonstrated a clear retrograde memory deficit contrasting with the preservation of anterograde memory and learning abilities. One year later, the autobiographic memory deficit was unmodified, except for what had been re-learnt. Brain MRI was normal while H20 brain PET scans demonstrated hypometabolism in the right globus pallidus and putamen after 2 weeks from onset, which was no longer present one year later. The absence of a clear pathomechanism underlying focal amnesia lead us to consider this case as an example of functional retrograde amnesia.

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Olfactory impairment is related to tau pathology and neuroinflammation in Alzheimer's disease

10.1101/2020.08.31.20183558 ◽

2020 ◽

Author(s):

Julia Klein ◽

Xinyu Yan ◽

Aubrey Johnson ◽

Zeljko Tomljanovic ◽

James Zou ◽

...

Keyword(s):

Brain Mri ◽

Temporal Cortex ◽

Posterior Cingulate Cortex ◽

Cognitive Status ◽

Odor Identification ◽

Amyloid Pet ◽

Tau Pathology ◽

Olfactory Impairment ◽

T Tau

Background: Olfactory impairment is evident in Alzheimers disease (AD), however, its precise relationships with in vivo measures of tau pathology and neuroinflammation are not well understood. Objective: To determine if odor identification performance measured with the University of Pennsylvania Smell Identification Test (UPSIT) is related to in vivo measures of tau pathology and neuroinflammation. Methods: Participants were selected from an established research cohort of adults aged 50 and older who underwent neuropsychological testing, brain MRI, and amyloid PET. Fifty-four participants were administered the UPSIT. Forty-one underwent 18F-MK-6240 PET and fifty-three underwent 11C-PBR28 PET to measure tau pathology and neuroinflammation, respectively. Twenty-three participants had lumbar puncture to measure CSF concentrations of total tau (t-tau), phosphorylated tau (p-tau) and beta;-amyloid (AB42). Results: Low UPSIT performance was associated with greater18F-MK-6240 binding in medial temporal cortex, hippocampus, middle/inferior temporal gyri, inferior parietal cortex and posterior cingulate cortex (p < 0.05). Similar relationships were seen for 11C-PBR28. These relationships were primarily driven by amyloid-positive participants. Lower UPSIT performance was associated with greater CSF concentrations of t-tau and p-tau (p < 0.05). Amyloid status and cognitive status exhibited independent effects on UPSIT performance (p < 0.01). Conclusions: Olfactory identification deficits are related to extent of tau pathology and neuroinflammation, particularly in those with amyloid pathophysiology. That amyloid-positivity and cognitive impairment are independently associated with odor identification suggests that low UPSIT performance may signify risk of AD pathophysiology in cognitively normal individuals and that impaired odor identification is associated with AD and non-AD-related neurodegeneration.

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Canine and feline vestibular syndrome

Journal of the Hellenic Veterinary Medical Society ◽

10.12681/jhvms.15011 ◽

2017 ◽

Vol 57 (1) ◽

pp. 63

Author(s):

Z. S. POLIZOPOULOU (Ζ. Σ. ΠΟΛΥΖΟΠΟΥΛΟΥ) ◽

A. M. DANOURDIS (Α. Μ. ΔΑΝΟΥΡΔΗΣ) ◽

A. F. KOUTINAS (Α. Φ. ΚΟΥΤΙΝΑΣ)

Keyword(s):

Complete Blood Count ◽

Brain Mri ◽

Head Tilt ◽

Vestibular Nuclei ◽

Serum Biochemistry ◽

Vestibular Dysfunction ◽

Point Of View ◽

Spontaneous Nystagmus ◽

Initial Assessment ◽

Cranial Nerve Dysfunction

Signs of vestibular dysfunction (head tilt, asymmetric ataxia, spontaneous nystagmus, unilateral falling and rolling) are characteristic enough to be easily recognized without difficulty, even by inexperienced clinicians. Further differentiation between the peripheral (inner ear, vestibular nerve) and the central (vestibular nuclei, cerebellar peduncles, fastigial nucleus and flocculonodular lobe of the cerebellum) vestibular system should be based on a thorough history and an astute neurological examination. Affected animals should be reevaluated by serial neurological reexaminations to improve the accuracy of the initial assessment. Concomitant neurological signs, such as spastic hemiparesis or tetraparesis, proprioceptive déficits, other cranial nerve dysfunction and/or behavioral changes are indicative of central than peripheral vestibular syndrome. Apart from the minimum data base (complete blood count, serum biochemistry, urinalysis), the diagnostic evaluation should also include otoscopy, plain radiography of tympanic bullae (peripheral vestibular lesions), ear CT, brain MRI and cererebrospinal fluid analysis (central vestibular lesions). The present review first describes the clinical features of the vestibular syndrome from a differential point of view, regarding its neuroanatomical origin and secondly the most common conditions primarily characterized by vestibular dysfunction in the dog and cat.

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