Creutzfeld-Jacob like syndrome due to lithium toxicity.

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J Neurol Neurosurg Psychiatry. 1989 February; 52(2): 291.
PMCID: PMC1032531

Creutzfeld-Jacob like syndrome due to lithium toxicity.


[Creutzfeldt-Jakob like syndrome due to lithium intoxication–a case report].

Rinsho Shinkeigaku. 1997 Apr;37(4):338-40.
[Article in Japanese]


Department of Neurology, Tenri Hospital.


A woman with mania who had been treated with lithium carbonate since 69 years of age presented mild tremulousness of both hands at the age of 76 years. She subsequently developed dysphagia, dysarthria, unsteady gait and progressive deterioration of the higher cortical function over 1.5 months. Her tremulousness deteriorated until it resembled myoclonus. EEG showed periodic sharp wave complexes appearing predominantly over the bilateral parieto-occipital areas. Although the EEG abnormality was not identical with that usually observed in the fully developed stage of Creutzfeldt-Jakob disease (CJD), it was reminiscent of that seen in the early stage of CJD. Thus, her clinical symptoms and signs were considered to resemble those of CJD. The plasma concentration of lithium, however, was found to be over the therapeutic range. Reduction of the dose of lithium carbonate almost completely resolved her symptoms within 3 weeks. Consequently, her clinical condition was considered lithium intoxication. Antidepressant and bismuth as well as lithium have been reported to induce a Creutzfeldt-Jakob like syndrome. Awareness of drug-induced Creutzfeldt-Jakob like syndrome is clinically important because of its excellent prognosis as opposed to the ominous prognosis of CJD.

[PubMed – indexed for MEDLINE]

Drug-induced Creutzfeldt-Jakob like syndrome.

J Psychiatry Neurosci. 1992 September; 17(3): 103–105.
PMCID: PMC1188422
Department of Neurology, Hahnemann University, Philadelphia, Pennsylvania.
This article has been cited by other articles in PMC.


A patient with progressive neurological deterioration characterized by cognitive impairment, myoclonus, Parkinson’s syndrome, an abnormal electroencephalogram and fasciculations was considered for brain biopsy for suspected Creutzfeldt-Jakob disease. Complete clinical recovery followed discontinuation of lithium and nortriptyline. Awareness of this unusual drug-induced Creutzfeldt-Jakob like syndrome can avoid costly, invasive and unnecessary investigative procedures.

Creutzfelt-Jakob disease presenting hyperparathyroidism.

Auris Nasus Larynx. 2000 Jul;27(3):281-3.


Department of Otolaryngology, Tochigi National Hospital, Tochigi, Japan.


We reported a 68-year-old female with Creutzfelt-Jakob disease (CJD) presenting hyperparathyroidism. She was suspected as Creutzfelt-Jakob like syndrome at her initial visit to our hospital because of progressive dementia and high level of serum calcium. Finally she was diagnosed as having CJD by the clinical symptoms including progressive dementia and myoclonus and the characteristic patterns of brain CT and electroencephalogram (EEG). CJD presents a variety of symptoms including progressive dementia, apathy and myoclonus. Hyperparathyroidism and toxicity of lithium, delirium and bismuth have been reported to induce similar symptoms of CJD, which are called Creutzfelt-Jakob like syndrome. Therefore, the diagnosis of CJD would be difficult in cases with CJD accompanied with Creutzfelt-Jakob like syndrome. It is rare for otolaryngologists to examine patients with dementia like CJD. However, we have to keep CJD in mind in the diagnosis of hyperparathyroidism.

[PubMed – indexed for MEDLINE]

[Lithium-induced encephalopathy mimicking Creutzfeldt-Jakob disease].

Rev Neurol (Paris). 2006 Nov;162(11):1118-21.
[Article in French]


Service de Neurologie et Pathologie du Mouvement, EA 2683, Hôpital Roger Salengro, rue du Professeur Emile Laine, CHRU, 59037 Lille Cedex.



Creutzfeldt-Jakob disease (CJD) has a poor prognosis. Certain clinical presentations can be suggestive yet mimic a curable disease.


In the present study, we report the case of a 67-year-old man with a one-month history of progressive dementia, with myoclonic jerks and cerebellar syndrome suggesting a diagnosis of Creutzfeldt-Jakob encephalopathy. He had been treated for 9 years with lithium for a bipolar disorder. The results of the different investigations and the favorable course after discontinuation of lithium were in favor of the diagnosis of drug-induced Creutzfeldt-Jakob syndrome.


This case illustrates the importance for researching a curable etiology in presence of clinical features suggesting a CJD.

[Psychiatric manifestations of a new variant of Creutzfeldt-Jakob disease. Apropos of a case].

Uploaded by on Feb  7, 2011

Elizabeth has a genetic form of Creutzfeldt-Jakob disease (CJD) and Colin’s wife was diagnosed with sporadic CJD in 2006. They explain how it affects their lives

Encephale. 2001 Mar-Apr;27(2):194-7.
[Article in French]


Service de Psychiatrie, BP 27, Centre Hospitalier Général, F-91401 Orsay.


The new variant of Creutzfeldt-Jakob disease (nvCJD) was first described in the UK in 1996 (16). The nvCJD differs from sporadic, genetic and iatrogenic CJD. Creutzfeldt-Jakob disease is closely associated with an abnormal isoform PrPSc of a cell-surface glycoprotein, prion protein (14). Molecular analysis suggests that nvCJD is caused by the same prion strain as bovine spongiform encephalopathy (BSE) (4, 10). To the end of September 2000, there have been 82 cases of nvCJD in the UK. We report the second French case of nvCJD to our knowledge (5, 13).


This 36 year old woman was referred by a local general practitioner with a 6 month history of psychiatric symptoms of major depressive disorder. According to her family, the patient had suffered from personality change for several months before the onset of depression including apathy, emotional lability, infantile affect. There was no history of health problems. As she was admitted to the psychiatric department of our hospital in Paris suburbs, she presented a major depressive disorder. There were no specific psychiatric features allowing distinction from common depressive disorders, except a marked emotional lability. The patient’s condition progressed rapidly within the following days. She presented memory impairment and disorientation. Drug treatments, clomipramine (125 mg/day) and venlafaxine (200 mg/day), were used with no benefit. She presented subsequently transient delusions and auditory hallucinations, fleeting for some hours. The predominant delusional themes were somatic type and pregnancy. The delusions were concomitant with delusions of the onset of cognitive impairment. The patient tested negative for the P 14.3.3 protein in the CSF. Computed tomography scan of the brain did not show any relevant abnormality. The electroencephalogram showed non specific slow wave activity. The neurological symptoms developed 7 months after the onset of depressive symptoms including ataxia, myoclonus, excessive daytime drowsiness, headache. After the onset of neurological symptoms, the illness progressed rapidly over the next 2 months with cognitive impairment, particularly memory impairment, myoclonus, ataxia, incontinence of urine and progressive immobility leading to dependency. CSF tests were negative. She was referred to a neurology department where the diagnosis was confirmed by brain biopsy (detailed elsewhere). The patient died in a state of akinetic mutism.


The clinical features of our patient were consistent with previous descriptions of nvCJD, mainly those of the National CJD Surveillance Unit studies (17): early psychiatric symptoms, prolonged duration of illness (median: 14 months), earlier age at death, compared with sporadic CJD. Psychiatric symptoms occur in the clinical course in about a third of cases of sporadic CJD (3). In contrast, of the 35 cases that have died of nvCJD identified in the study by Will et al. (17), 34 suffered from early and prominent psychiatric symptoms, mainly depression and anxiety. In most of the patients, the first symptoms were psychiatric. Drug treatment was used in most cases, some patients had a transient improvement (18). The patient without psychiatric symptoms reported by the NCJDSU (17) was emotionally labile. Infantile affect and emotional lability, found in our patient, are frequently reported in other studies (1, 18). Schizophreniform disorders have been described during the clinical course, with auditory and visual hallucinations and paranoid delusions (17, 18). The insomnia and excessive daytime drowsiness our patient presented have been described in similar cases (18). Investigations are important to rule out alternative diagnoses. EEG records do not show periodic triphasic complexes as in sporadic CJD. The P 14.3.3 protein in the CSF is positive in half the cases of nvCJD (17). First neurological symptoms developed 6 months after the onset of psychiatric symptoms including ataxia, myoclonus and persistent painful sensory symptoms (17, 18). In most of the cases, MRI brain scans show bilateral pulvinar high signal (17), found subsequently in our patient and detailed elsewhere (13). The terminal stages are progressive cognitive impairment, helplessness and akinetic mutism.


The first symptoms of this patient were purely psychiatric and difficult to distinguish from common psychiatric disorders. Clinical surveillance of human prion disease is crucial in France, as in UK. The link with BSE has dramatically highlighted the need for neurological and neuropsychological precise investigations.

Psychoses as the presenting manifestation of Creutzfeldt-Jakob disease in an elderly male

Gen Hosp Psychiatry. 2011 May-Jun;33(3):302.e7-9. Epub  2011 Mar 24.

Li X, Lapid MI, Burton MC, Josephs KA.


Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN 55905, USA.


The differential diagnosis of acute psychosis includes delirium, dementia and primary psychiatric disorders. A comprehensive medical evaluation is crucial to make the proper diagnosis. We report the case of a healthy elderly man who presents with acute psychosis. We describe our diagnostic evaluation based on the patient’s history and physical examination, which identified Creutzfeldt-Jakob disease. Avoiding diagnostic error in patients who face such a rapidly progressive and catastrophic illness is paramount.

Uploaded by on Jul  3, 2008

WTHR from Indianpolis aired this documentary in the Fall of 2006.  My brother was Zane Mingus.

A Creutzfeldt-Jakob like syndrome due to lithium toxicity.

J Neurol Neurosurg Psychiatry. 1988 January; 51(1): 120–123.
PMCID: PMC1032724

A Creutzfeldt-Jakob like syndrome due to lithium toxicity.


Two patients with lithium toxicity presented with a neurological syndrome suggesting a diagnosis of Creutzfeldt-Jakob disease. In both cases, the initial EEG was consistent with this diagnosis. Neither patient had permanent neurological sequelae and the EEG returned to normal. A careful drug history should be taken in any patient who presents with a rapidly progressive dementia even when the EEG supports a diagnosis of Creutzfeldt-Jakob disease.

Lithium-induced Creutzfeldt-Jakob syndrome.

Clin Neuropharmacol. 1996 Aug;19(4):356-9.


Department of Neurology, Hospital Universitari La Fe, Valencia, Spain.


a 67-year-old man with bipolar disorder developed a Creutzfeldt-Jakob like syndrome during lithium carbonate treatment. Lithium serum level was within the therapeutic range. Complete clinical-electroencephalographic recovery was achieved after lithium therapy was discontinued. Several cases of lithium-induced Creutzfeldt-Jakob syndrome have been reported to date; all of them were elderly patients and a half had “therapeutic” lithium serum levels. Patients in this age group receiving antimanic maintenance treatment should keep lithium serum levels as low as possible. Lithium neurotoxicity should be considered in Creutzfeldt-Jakob disease differential diagnosis, serial electroencephalograms being the most valuable.

[PubMed – indexed for MEDLINE]

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