scholarly journals Paroxysmal Amnesia Attacks due to Hashimoto’s Encephalopathy

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Pelin Nar Senol ◽  
Aylin Bican Demir ◽  
Ibrahim Bora ◽  
Mustafa Bakar

Hashimoto’s encephalopathy is a rare disease which is thought to be autoimmune and steroid responsive. The syndrome is characterized by cognitive impairment, encephalopathy, psychiatric symptoms, and seizures associated with increased level of anti-thyroid antibodies. The exact pathophysiology underlying cerebral involvement is still lesser known. Although symptoms suggest a nonlesional encephalopathy in most of the cases, sometimes the clinical appearance can be subtle and may not respond to immunosuppressants or immunomodulatory agents. Here we report a case who presented with drowsiness and amnestic complaints associated with paroxysmal electroencephalography (EEG) abnormalities which could be treated only with an antiepileptic drug.

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Lilibet Urias-Uribe ◽  
Emmanuel Valdez-Solis ◽  
Claudia González-Milán ◽  
Claudia Ramírez-Rentería ◽  
Aldo Ferreira-Hermosillo

We present the case of a patient with previous psychiatric illness, acutely exacerbated by thyroid storm due to Graves’ disease, in whom treatment with antipsychotics induced catatonia. These associations are extremely rare and may be confused with Hashimoto’s encephalopathy, especially in the presence of anti-thyroid antibodies in cerebrospinal fluid. The treatment consists in the control of the triggering disease (in this case the resolution of the thyrotoxicosis) and the use of benzodiazepines. However, in some cases, the resolution of psychiatric symptoms is partial and may require the use of electroconvulsive therapy.


2020 ◽  
Vol 13 (12) ◽  
pp. e233179
Author(s):  
Eric Garrels ◽  
Fawziya Huq ◽  
Gavin McKay

Limbic encephalitis is often reported to present as seizures and impaired cognition with little focus on psychiatric presentations. In this case report, we present a 49-year-old man who initially presented to the Psychiatric Liaison Service with a several month history of confusion with the additional emergence of visual hallucinations and delusions. Due to the inconsistent nature of the symptoms in the context of a major financial stressor, a provisional functional cognitive impairment diagnosis was made. Investigations later revealed a positive titre of voltage-gated potassium channel (VGKC) antibodies, subtype leucine-rich glioma inactivated 1 accounting for his symptoms which dramatically resolved with steroids and immunoglobulins. This case highlighted the need for maintaining broad differential diagnoses in a patient presenting with unusual psychiatric symptoms.


2015 ◽  
Vol 5 (1) ◽  
pp. 42-50 ◽  
Author(s):  
Antonella De Carolis ◽  
Virginia Cipollini ◽  
Valentina Corigliano ◽  
Anna Comparelli ◽  
Micaela Sepe-Monti ◽  
...  

Aims: To investigate, in a group of subjects at an early stage of cognitive impairment, the relationship between anosognosia and both cognitive and behavioral symptoms by exploring the various domains of insight. Methods: One hundred and eight subjects affected by cognitive impairment were consecutively enrolled. The level of awareness was evaluated by means of the Clinical Insight Rating Scale (CIRS). Psychiatric symptoms were evaluated using the Italian version of the Neuropsychiatric Inventory (NPI), whereas memory (memory index, MI) and executive (executive index, EI) functions were explored using a battery of neuropsychological tests and qualified by means of a single composite cognitive index score for each function. Results: A significant positive correlation between the total NPI score and global anosognosia score was found. Furthermore, both the MI and EI scores were lower in subjects with anosognosia than in those without anosognosia (p < 0.001 and p < 0.007, respectively). When the single domains of the CIRS were considered, anosognosia of reason of visit correlated with the EI score (r = -0.327, p = 0.01) and night-time behavioral disturbances (r = 0.225; p = 0.021); anosognosia of cognitive deficit correlated with depression (r = -0.193; p = 0.049) and the MI score (r = -0.201; p = 0.040); anosognosia of functional deficit correlated with the MI score (r = -0.257; p = 0.008), delusions (r = 0.232; p = 0.015) and aberrant motor behavior (r = 0.289; p = 0.003); anosognosia of disease progression correlated with the MI score (r = -0.236; p = 0.015), agitation (r = 0.247; p = 0.011), aberrant motor behavior (r = 0.351; p = 0.001) and night-time behavioral disturbances (r = 0.216; p = 0.027). Conclusions: Our study suggests that, in the early stage of cognitive impairment, anosognosia is associated with both cognitive deficits and behavioral disorders according to the specific functional anatomy of the symptoms.


2017 ◽  
Vol 2017 ◽  
pp. 1-3 ◽  
Author(s):  
Murugan Selvaraj Karthik ◽  
Kulothungan Nandhini ◽  
Viswanath Subashini ◽  
Ramasamy Balakrishnan

Hashimoto’s encephalopathy (HE) is a rare autoimmune disorder with neurological and neuropsychiatric manifestations and elevated titres of anti-thyroid antibodies. Here we are reporting a case of HE in a 19-year-old girl who presented with seizure-like episodes, confusion, and behavioural disturbances with catatonic symptoms such as posturing, echopraxia, echolalia, and ambivalence. Patient did not respond to antipsychotics and anticonvulsants. On further investigation, patient was found to have high serum anti-TPO antibodies of about 1261 U/mL with euthyroid status, which supported a suspicion of HE. Our consultant neurologist confirmed the diagnosis and she was started on injection of methylprednisolone 750 mg OD. Since patient started showing clinical improvement, her antipsychotic medications were tapered off. On follow-up, patient has recovered and is functioning well. Since HE is a diagnosis of exclusion, very high anti-TPO antibodies and good response to steroids supported the diagnosis of HE in this patient after excluding other etiological possibilities. This case has been reported because the clinical presentation was predominantly neurobehavioural manifestations which is uncommon with HE.


Reumatismo ◽  
2018 ◽  
Vol 70 (4) ◽  
pp. 268-269
Author(s):  
C. Cosso ◽  
M. Ghio ◽  
M. Cutolo

Hashimoto’s encephalopathy (HE) is an autoimmune form of encephalopathy, associated with autoimmune thyroiditis. Its prevalence is estimated to be 2:100,000. HE is characterized by behavioral changes, mental confusion, dysarthria, ataxia, psychosis, paranoia, convulsions, hallucinations, headache and hyperthermia. Elevated thyroid antibodies are necessary for diagnosis and the disease responds dramatically to glucocorticoid therapy. We describe a patient with HE and panniculitis, an association reported twice in the literature.


2019 ◽  
Vol 12 (11) ◽  
pp. e230011
Author(s):  
Timothy A Gregory ◽  
Gillian N Jones ◽  
Yince Loh

There are many examples in the literature of Hashimoto’s encephalopathy (HE) presenting with heterogeneous manifestations to include stroke-like episodes, seizures, myoclonus and psychiatric symptoms. The pathogenesis is poorly understood but is thought to involve an autoimmune-mediated vasculitis. Here, we present a novel case showing hemispheric hyperaemia which created a diagnostic challenge and insinuated a vascular mechanism for the condition. The patient presented with left-sided stroke-like symptoms and had head CT angiography notable for asymmetric vasculature initially interpreted radiographically as decreased left middle cerebral artery (MCA) flow. An MRI brain demonstrated right-sided holohemispheric fluid-attenuatedinversion recovery (FLAIR) hyperintensity with right insula contrast enhancement. She was found to have elevated anti-thyroid peroxidase (TPO) antibodies with an otherwise negative encephalitis workup. The patient was diagnosed with HE and acutely progressed to have focal seizures during a prolonged intensive care unit stay. She ultimately required intravenous Ig and antiepileptic medications to gain control of her disease. This case appears to be the first described presentation of hemiencephalitis with local hyperaemia, and may represent local autoregulatory loss as a result of vasculitis. This supports the existing literature implicating inflammatory microvascular infiltration in the mechanism of the disease. HE must be considered in a broad range of unexplained neurological symptoms.


2010 ◽  
Vol 1 (1) ◽  
pp. 3 ◽  
Author(s):  
Vicky Chau ◽  
Sadhana Prasad ◽  
Dwight Stewart ◽  
George Heckman

Patients with Creutzfeldt–Jakob disease (CJD) may exhibit characteristic abnormalities on the electroencephalogram (EEG). However, these abnormalities have been associated with a number of cases of drug toxicity. We report a case of CJD-like syndrome associated with gabapentin. A 78-year-old man was hospitalized for recurrent falls. Three months prior to admission, gabapentin was prescribed to treat symptoms of trigeminal neuralgia. The patient subsequently presented with a two-month history of worsening gait abnormalities, negative myoclonus, and cognitive impairment. The EEG showed diffuse background slowing with larger amplitude delta discharges, which at times appeared triphasic, raising the possibility of CJD. The gait abnormalities and myoclonus resolved and the EEG normalized after the gabapentin was discontinued. Several cases of drug-induced CJD-like syndrome have been reported, mainly presenting with cognitive impairment, myoclonus, Parkinsonism, and EEG abnormalities. This patient may have been predisposed to adverse neurological effects from gabapentin owing to age, concurrent renal insufficiency, and cardiac disease. We concluded that it is imperative to include drug toxicity in the differential diagnosis of patients presenting with clinical manifestations and EEG findings suggestive of CJD, particularly in the setting of advanced age and comorbidities.


2020 ◽  
Vol 11 (3) ◽  
pp. 198-199
Author(s):  
Tommaso Ercoli ◽  
Federica Maria Genitori ◽  
Giovanni Defazio ◽  
Antonella Muroni

2018 ◽  
Vol 49 (6) ◽  
pp. 881-890 ◽  
Author(s):  
Nicole N. Lønfeldt ◽  
Frank C. Verhulst ◽  
Katrine Strandberg-Larsen ◽  
Kerstin J. Plessen ◽  
Eli R. Lebowitz

AbstractExperts have raised concerns that oxytocin for labor induction and augmentation may have detrimental effects on the neurodevelopment of children. To investigate whether there is the reason for concern, we reviewed and evaluated the available evidence by searching databases with no language or date restrictions up to 9 September 2018. We included English-language studies reporting results on the association between perinatal oxytocin exposure and any cognitive impairment, psychiatric symptoms or disorders in childhood. We assessed the quality of studies using the Newcastle–Ottawa Quality Assessment Scales. Independent risk estimates were pooled using random-effects meta-analyses when at least two independent datasets provided data on the same symptom or disorder. Otherwise, we provided narrative summaries. Two studies examined cognitive impairment, one examined problem behavior, three examined attention-deficit/hyperactivity disorder (ADHD) and seven focused on autism spectrum disorders (ASD). We provided narrative summaries of the studies on cognitive impairment. For ADHD, the pooled risk estimate was 1.17; 95% confidence interval (CI) 0.77–1.78, based on a pooled sample size of 5 47 278 offspring. For ASD, the pooled risk estimate was 1.10; 95% CI 1.04–1.17, based on 8 87 470 offspring. Conclusions that perinatal oxytocin increases the risks of neurodevelopmental problems are premature. Observational studies of low to high quality comprise the evidence-base, and confounding, especially by the genetic or environmental vulnerability, remains an issue. Current evidence is insufficient to justify modifying obstetric guidelines for the use of oxytocin, which state that it should only be used when clinically indicated.


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