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<p><i>Creutzfeldt–Jakob disease (CJD)</i> is a rare and fatal neurodegenerative disorder caused by misfolded prion proteins. It progresses inexorably to death once clinical symptoms emerge. Early manifestations are often nonspecific and may mimic other neurological conditions, making diagnosis particularly challenging.</p><p> We report the case of a 54-year-old Palestinian male who initially presented with dysarthria, vertical gaze nystagmus, dizziness, and gait ataxia while maintaining preserved cognition. Over the following month, he developed short-term memory loss, hallucinations, and disorientation. Extensive workup excluded infectious, toxicological, autoimmune, metabolic, and paraneoplastic causes. Cerebrospinal fluid (CSF) analysis revealed markedly elevated tau protein, a decreased Aβ42/40 ratio, and positive 14-3-3 protein. Although the initial Magnetic Resonance Imaging (MRI) was unremarkable, a follow-up scan demonstrated bilateral thalamic and basal ganglia abnormalities. Trials of plasmapheresis and corticosteroids were administered without clinical improvement. The patient's condition deteriorated rapidly, culminating in death within seven months of symptom onset. This case of CJD was considered the first to be documented in Palestine.</p>

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Sporadic Creutzfeldt–Jakob disease in Palestine with early ataxia and dysarthria: a case report

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月2日

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  • Anita S. Bahbah,
  • Esra’a O. Kurdi,
  • Darwish M. Mosameh,
  • Baraa M.M. Sharawi,
  • Mohammed Damrah

摘要

Creutzfeldt–Jakob disease (CJD) is a rare and fatal neurodegenerative disorder caused by misfolded prion proteins. It progresses inexorably to death once clinical symptoms emerge. Early manifestations are often nonspecific and may mimic other neurological conditions, making diagnosis particularly challenging.

We report the case of a 54-year-old Palestinian male who initially presented with dysarthria, vertical gaze nystagmus, dizziness, and gait ataxia while maintaining preserved cognition. Over the following month, he developed short-term memory loss, hallucinations, and disorientation. Extensive workup excluded infectious, toxicological, autoimmune, metabolic, and paraneoplastic causes. Cerebrospinal fluid (CSF) analysis revealed markedly elevated tau protein, a decreased Aβ42/40 ratio, and positive 14-3-3 protein. Although the initial Magnetic Resonance Imaging (MRI) was unremarkable, a follow-up scan demonstrated bilateral thalamic and basal ganglia abnormalities. Trials of plasmapheresis and corticosteroids were administered without clinical improvement. The patient's condition deteriorated rapidly, culminating in death within seven months of symptom onset. This case of CJD was considered the first to be documented in Palestine.