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Parkinson’s disease who possiblyexhibits this rare form of percep-tual disturbance.

Case Report

Our patient is a 76-year-old Cauca-

sian woman with a 3-year history ofParkinson’s disease, presenting withacute dyspnea which resulted in herhospitalization. She reported visualhallucinations of “mechanical bugswalking around the hospital” and“two people fighting” in the cornerof her room. The visual hallucina-tions began 1 year prior to her hos-pitalization and were nondistressing.She had insight into the visual hallu-cinations. Our patient was treated

with carbidopa-l-dopa until 4months prior to admission. Thepatient’s mental status exam wasnotable for bradyphasia, psychomo-tor retardation, and limited range ofaffect. She had signs of a pill rollingtremor on her left hand. She wasotherwise alert and oriented times 3with no fluctuations in conscious-ness. She reports visual hallucina-tions in the absence of bizarre delu-sions or auditory hallucinations.

Cognitive examination was notablefor deficits in short-term recall(which improved with cues) andattention span.

An MRI scan of the brainrevealed a hyper-intense focusadjacent to the right thalamus con-sistent with an old lacunar infarct.An EEG revealed no eliptiform dis-charges or significant slowing.

Our patient was treated withquetiapine for the visual hallucina-tions, with a noted decrease in the

number of hallucinations for theremainder of the hospital stay.

Discussion

Visual hallucinations often suggesta wide range of etiologies. Halluci-nations and delusions occur in upto 40% of patients with Parkinson’sdisease. Visual hallucinations aretypically associated as a side effect

of dopamine agonists, such as car- bidopa-l-dopa, in about 20% ofParkinson’s disease patients; how-ever, our patient’s visual hallucina-tions persisted despite discontinua-tion of carbidopa-l-dopa.2 The

differential diagnosis for visual hal-lucinations includes neurodegen-erative dementias, such as Parkin-son’s dementia, postictal states,intoxications/delirium tremens,migraine headache with aura, andnarcolepsy.3

Peduncular hallucinosis is a rareform of visual hallucination charac-terized by intense, vividly colored,nonstereotypical visual images ofpeople, animals, and plants that are

nonthreatening to the patient. Theexact mechanism for peduncularhallucinosis is unknown. Onetheory is that when “normal” affer-ent input is decreased, for example by diminished visual acuity, spon-taneous cerebral activity of thevisual system is disinhibited,resulting in visual hallucinations.However, given the rarity of suchcases, it may be that cerebralpathology may render some elderly

patients vulnerable to this disinhib-ited phenomena associated withpontine lesions.4 However, accord-ing to Cubo et al.,5 visual halluci-nations are more likely to occurwith more severe overall Parkin-son’s symptoms and longer dura-tion of Parkinson’s disease. Ourpatient only had Parkinson’s dis-ease for 3 years and was onlymildly impaired by the illness.Thus, based on clinical and radio-graphic findings, peduncular hallu-

cinosis was considered in the dif-ferential diagnosis of our patient’svisual hallucinations. In closing, theemergence of new-onset visual hal-lucinations in the elderly warrantsan MRI of the brain and, althoughrare, peduncular hallucinosisshould be considered in the differ-ential diagnosis, especially with brain stem or thalamic infarcts.

David R. Spiegel, M.D.

Brandy Lybeck, B.S.

Victoria Angeles, M.D.

Department of Psychiatry,Eastern Virginia MedicalSchool, Norfolk, Virginia

References

1. Leo RJ, Aherens KS: Visual hallucina-tions in mild dementia: a rare occurrenceof Lhermitte’s hallucinosis. Psychosomat-ics 1999; 40:360–363

2. Cummings JL, Miller BL: Visual halluci-nations: clinical occurrence and use indifferential diagnosis. West J Med 1987;146:46–51

3. Marsh L: Neuropsychiatric aspects ofParkinson’s disease. Psychosomatics1999; 41:15–23

4. Feinberg WM, Rapcsak SZ: Peduncularhallucinosis following paramedian tha-lamic infarction. Neurology 1989;39:1535–1536

5. Cubo E, Gonzalez M, Aguilar A, et al:[Study of associated clinical variablesand phenomenology of hallucinations inParkinson’s.] Neurologia 2006; 21:12–18(Spanish)

The Role of Melatonin in

Sleep Disturbances in End-Stage Huntington’s Disease

To the Editor: Sleep disturbances arecommon in Huntington’s diseaseand are often characterized by dis-ruption of day-night patterns.1–3 Ingeneral, these sleep disturbancesare attributed to factors of comor- bidity (depression, mania), medica-tion, or specific symptoms such as

chorea or dystonia.Circadian sleep is regulated by

the “biological clock” or “pace-maker” of the suprachiasmaticnucleus. This pacemaker stimulatesmelatonin synthesis in the pinealgland. Clock genes play a centralrole in this molecular oscillationprocess. In an animal model ofHuntington’s disease, a marked

LETTERS

226226 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 21:2, Spring 2009

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disruption of expression of theclock genes mPer2 and mBal wasfound in the suprachiasmaticnucleus.3 This may have negativeconsequences for the production ofmelatonin and the circadian sleep

rhythm.We evaluated the occurrence of

circadian sleep disorders in end-stage Huntington’s disease bydetermining deviations of dim lightmelatonin onset out of the saliva of10 Huntington’s disease patientswith a sleep disorder according toDSM-IV-TR criteria. Patients wereall residents in a specialized Hun-tington’s disease ward of a nursinghome who required constant care

 because of the severity of their dis-ease.

Dim light melatonin onset is themost accurate marker for assessingthe circadian pacemaker. It isdefined as the time at which a sali-vary concentration of 4 pg/ml isreached.4 Normally, this concentra-tion is reached in adults between7:30 p.m. and 10:00 p.m.5 Dim lightmelatonin onset was determined byobtaining hourly saliva samples

(from 9:00 p.m. to 1:00 a.m.) bychewing on a cotton plug for 1minute (Salivetten, Sarstedt Etten-Leur, the Netherlands). Because ofthe risk of choking the researcherused a plastic clip to hold thecotton plug in place in the patient’smouth. In the evening, patientswere held to food restrictions andwere requested to avoid physicalstrain and bright light. Normalmedication use was continued tomaintain therapeutic blood levels

and to avoid disruption of normalroutine.

Dim light melatonin onset wasidentified in five of the 10 patients.One patient reached the melatoninconcentration of 4 pg/ml in saliva before 10:00 p.m. In four of the fivepatients, dim light melatonin onsetwas identified between 10:00 p.m.and 12:00 a.m. One patient did not

reach the concentration of 4 pg/ml before 1:00 a.m. In one patient,melatonin could not be detected insaliva samples, and in another, themelatonin assessment failed due toan insufficient quantity of saliva.

Two patients dropped out. Whendim light melatonin onset datawere combined with circadiansleep disturbances, we found twopatients with delayed sleep symp-toms with dim light melatoninonset between 10:00 p.m. and 12:00a.m. One patient (with undetect-able saliva melatonin) showedadvanced sleep symptoms.

In conclusion, although sleepresearch is difficult in severe end-

stage Huntington’s disease, theresults of our study did providesome support for the hypothesisthat there is a relation betweenHuntington’s disease and circadiansleep disturbances that could becaused by melatonin deficiency.Further research using an experi-mental treatment with melatonin ina placebo-controlled setting is rec-ommended.

 Judith Alders, M.D.

GG-Net, Centre for MentalHealth, Apeldoorn, The Neth-erlands

Marcel Smits, M.D., Ph.D.

Department of Neurology andSleep Disorders, GelderseVallei Hospital, Ede, The Neth-erlands

Berry Kremer, M.D., Ph.D.

Neurology, Radboud Univer-sity Nijmegen, Medical Centre,Nijmegen, The Netherlands

Paul Naarding, M.D., Ph.D.

Psychiatry, GG-Net, Centre forMental Health, Apeldoorn, TheNetherlands

References

1. Wiegand M, Moller AA, Lauer CJ, et al:Nocturnal sleep in Huntington’s disease: J Neurol 1991; 238:203–208

2. Hansotia P, Wall R, Berendes J: Sleep

disturbances and severity of Hunting-ton’s disease. Neurology 1985; 35:1672–164

3. Morton AJ, Wood NI, Hastings MH, etal: Disintegration of the sleep-wake cycleand circadian timing in Huntington’sdisease. J Neurosci 2005; 25:157–163

4. Pandi-Perumal SR, Smits M, Spence W,et al: Dim light melatonin onset (DLMO):a tool for the analysis of circadian phasein human sleep and chronobiological dis-orders. Prog Neuropsychopharmacol BiolPsychiatry 2007; 31:1–11

5. Nagtegaal JE, Kerkhof GA, Smits MG, etal: Delayed sleep phase syndrome: a pla-cebo-controlled cross-over study on theeffects of melatonin administered fivehours before the individual dim lightmelatonin onset. J Sleep Res 1998; 7:135–143

Co-occurrence of X-Linked

Congenital Adrenal

Hypoplasia and Autistic

Disorder

To the Editor: One form of congeni-tal adrenal hypoplasia is associatedwith the Xp21 chromosomal region.These patients have clinical abnor-malities including mental retarda-tion, hearing loss, hypogonadism,glycerol kinase deficiency, ornithinetranscarbamoylase deficiency, andDuchenne muscular dystrophy.This letter presents a case of apatient with X-linked congenitaladrenal hypoplasia whose mentalstatus as a preadolescent male wasalso consistent with the diagnosisof autistic disorder.

Case ReportA 12-year-old Caucasian boy pre-sented with features of autistic dis-order including marked lack ofawareness of the feelings of others;no seeking of comfort in times ofdistress; gross impairment in abil-ity to make peer friendships;abnormal nonverbal communica-tion; abnormalities in speech pro-

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