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Case Report

Dogan, et al.: A case of peduncular hallusinosis

A case of peduncular hallucinosis presenting as a primary psychiatric disorder Vasfiye Burcu Dogan, Ayten Dirican, Ayhan Koksal, Sevim Baybas Department of Neurology, Bakırkoy Research and Training Hospital for Neurologic and Psychiatric Diseases, Istanbul, Turkey Abstarct Peduncular hallucinosis usually occurs due to vascular or infectious midbrain lesions or brain stem compression by tumors. We present a peduncular hallucinosis case in a 63‑year‑old female with brain stem infarction, which can easily be misdiagnosed as a psychiatric disorder.

Key Words Cerebrovascular accident, peduncular hallucinosis, midbrain For correspondence: Dr. Vasfiye Burcu Dogan, Department of Neurology, Bakırkoy Research and Training Hospital for Neurologic and Psychiatric

Diseases, Istanbul, Turkey. E‑mail: [email protected]

Ann Indian Acad Neurol 2013;16:684‑6

Introduction Peduncular Hallucinosis is a rare case which was firstly reported by L’Hermitte. It is characterized by complex, colorful, visual, combined visual‑acustic or visual‑tactile hallucinations. It often occurs due to vascular lesions, infections and tumors of brain stem.

Case Report A 63‑year‑old female patient was admitted to the psychiatry emergency clinic for hallucinations, nervousness and agitation, which had started abruptly before 2 days. She was described to be a little bit aggressive and conversable person before but neither the patient nor her family had a previous history of psychiatric disease. She was consulted to neurology as a late‑onset psychiatric disorder to rule out an organic etiology. She had hypertension and had an ischemic cerebrovascular accident before and stopped taking acetylsalicylic acid treatment for 3 days. Before 2 days, she had suddenly seen her sister was plastering the house she lived before and it had lasted nearly 5‑6 min. Access this article online Quick Response Code:

Website: www.annalsofian.org

DOI: 10.4103/0972-2327.120469

After a few hours later, she had seen her dead mother calling her “come here’’ and this also had lasted nearly 5‑6 min. After several hours, she had heard some voices calling “get out and walk’’ and she had walked aimlessly in the house. Then, she had become agitated and had thrown her grandson’s toys around and had broken a window. After that she had attempted to jump down from the balcony and had slapped her daughter’s face while she was trying to hold her. After she had calmed down, she had recognized these all as hallucinations and her children had brought her to the psychiatry emergency clinic. At the neurological examination, she was cooperative, orientation for the person and the location was normal, but she was disoriented to time and couldn’t distinguish night and day. Cranial nerves were intact; there was no paresia other than a left upper monoparesia, which was the sequel of a previous ischemic cerebrovascular accident. She was aware of the hallucinations that she had. There was no metabolic abnormality in blood examination; electrocardiogram and electroencephalogram  (EEG) was normal, no acute pathology was found in cranial computed tomography. Acute infarction was found at the left side of pons with diffusion weighted magnetic resonance imaging (MRI) investigation [Figures 1 and 2]. She was diagnosed as a cerebrovasculer accident presenting with pedincular hallucinosis and was treated with heparin and 100 mg/day acetyl salicylic acid and ketiapin 50 mg/day was given for hallucinations. One week later, her hallucinations were resolved almost completely.

Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4

Dogan, et al.: A case of peduncular hallusinosis

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Figure 1: Diffusion magnetic resonance imaging of acute left pons infarct, showed with arrow

Figure 2: Diffusion magnetic resonance imaging of the same pons infarct, showed with arrow

Discussion

tremor or autonomic impairment and orientation was intact for the person and location. There wasn’t any headache consistent with migraine. We also excluded Charles Bonnet syndrome because there was no visual field defect or visual impairment. Schizophrenia and other psychotic illnesses were excluded because she was normal between hallucinations. There was not laboratory and physical finding and history for any kind of hallucinogen agent such as Lysergic acid diethylamid LSD, cocaine and amphetamine. Epileptic seizures were also excluded for EEG was normal during these hallucinations.

Peduncular Hallusinosis PH is a rare, but interesting entity, so it’s a well‑known phenomenon. L’Hermitte, first reported a PH case at a 72‑year‑old female patient. Her symptoms were headache, nausea, vomiting, vertigo and these were followed by the left eye ptosis, external ophtalmoplegia, ataxia and hallucinations consisting of wild animals, colorful interesting suited people, children playing games.[1] PH often occurs due to intrinsic vascular lesions of brainstem, but may occur due to infections, tumors, and after vertebral artery angiography.[2‑7] PH is characterized by complex, naturalistic, colorful, mostly visual, but also combined visual‑acoustic or visual‑tactile hallucinations and also by behavioral abnormalities occurring due to upper brainstem and thalamic lesions.[3,8,9] These hallucinations usually start within a few days of the initial insult and resolve within a few weeks, but they may last for years. Each hallucination may last from minutes to hours, often occurring in the evening.[2] Our patient’s hallucinations were repetitive, both visual and acoustic and lasted nearly for 5‑6 min and could be described as complex visual hallucinations. Although complex visual hallucinations are usually unimodal, they can be rarely polymodal as in our case.[10] Complex visual hallucinations may be seen in a variety of disorders and must be considered at the differential diagnosis of PH. These consist of narcolepsy‑cataplexy syndrome, Parkinson’s disease, Lewy body dementia, delirium, migraine coma, Charles Bonnet syndrome, Schizophrenia, hallucinogen induced states and epilepsy.[10] Narcolepsy‑cataplexy syndrome was excluded because her hallucinations were not related to sleep and cataplexy. We didn’t think Parkinson’s disease for there were no extrapyramidal findings at neurologic examination. Although her time orientation was impaired and she couldn’t distinguish night and the day, we didn’t think Lewy body dementia because her location and person orientation were intact and there was no cortical atrophy consistent with dementia at cranial MRI. Delirium was also excluded for there was not

Pathophysiology of peduncular hallucinosis is not well‑known, but L’Hermitte suggested that Rapid Eye Movement REM activity release phenomenon may be the cause.[1] There is no enough evidence that these hallucinations are due to visual field or tract destruction. Manford and Andermann reported two peduncular hallucinosis cases with thalamic and brainstem infarcts, and both have had normal visual field examinations and visual evoked potentials. [10] Even if pathophysiology is not well‑known yet, it is known that reticular activating system destruction is responsible for peduncular hallucinosis.[10,11] Our case with brainstem infarction had no neurological deficit other than peduncular hallucinations. For this reason, organicity must be ruled out in an elderly person with no previous history or family history of psychiatric diseases presenting with psychiatric symptoms for the first time. We report this case to underline the importance of organicity in PH because it may be overlooked easily and misdiagnosed as a psychiatric disorder.

References 1. Lhermitte J. Syndrome de la calotte du pedoncule cérébral. Les troubles psycho‑sensoriels dans les lesions du mésocéphale. Rev Neurol 1922;2:1359‑65. 2. Ryan C, Teeple BS, Jason P, Caplan MD, Theodore A, Stern MD. Visual hallucinations: Differential diagnosis and treatment. J Clin Psychiatry 2009;11:26‑32. 3. Dunn DW, Weisberg LA, Nadell J. Peduncular hallucinations caused by brainstem compression. Neurology 1983;33:1360‑1.

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Dogan, et al.: A case of peduncular hallusinosis

4. Nadvi SS, van Dellen JR. Transient peduncular hallucinations secondary to brain stem compression by a medulloblastoma. Surg Neurol 1994;41:250‑2. 5. Rozanskı J. Peduncular hallucinosis following vertebral angiography. Neurology 1952;2:341‑9. 6. Nadvi SS, Ramdial PK. Transient peduncular hallucinations secondary to brain stem compression by a cerebellar pilocytic astrocytoma. Br J Neurosurg 1998;12:579‑81. 7. McKee AC, Levine DN, Kowall NW, Richardson EP Jr. Peduncular hallucinosis associated with isolated infarction of the substantia nigra pars reticulata. Ann Neurol 1990;27:500‑4. 8. Feinberg WM, Rapcsak SZ. ‘Peduncular hallucinosis’ following paramedian thalamic infarction. Neurology 1989;39:1535‑6. 9. De Morsier G. Pathogenic de L’hallucinose pedonculaire: A propos

d’un nouveaucas. Rev Neurol (Paris) 1935;64:606‑8. 10. Manford M, Andermann F. Complex visual hallucinations. Clinical and neurobiological insights. Brain 1998;121:1819‑40. 11. Serra Catafau J, Rubio F, Peres Serra J. Peduncular hallucinosis associated with posterior thalamic infarction. J Neurol 1992;239:89‑90. How to cite this article: Dogan VB, Dirican A, Koksal A, Baybas S. A case of peduncular hallucinosis presenting as a primary psychiatric disorder. Ann Indian Acad Neurol 2013;16:684-6. Received: 06‑01‑13, Revised: 27‑03‑13, Accepted: 21‑04‑13

Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4

Source of Support: Nil, Conflict of Interest: Nil

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A case of peduncular hallucinosis presenting as a primary psychiatric disorder.

Peduncular hallucinosis usually occurs due to vascular or infectious midbrain lesions or brain stem compression by tumors. We present a peduncular hal...
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