History Of Visual Hallucinations Research Articles

Challenges in Diagnosing Functional Visual Loss and Malingering: a Case Report

Abstract
 Introduction : Functional Visual Loss (FVL) is decreased visual acuity and/or altered visual fields without any associated organic pathology and is considered within the spectrum of malingering. It manifests as either simulating an ophthalmic disease or denying ophthalmic disease. Thorough history-taking and careful examination of the patient are essential in reaching the diagnosis.
 Case Illustration : A 17-year-old female came with complaints of a spinning headache, sudden and painless blurry vision in both eyes, double vision, and a history of syncope for the last two days. Ophthalmology examination revealed UCVA was 0.5/60 for both eyes with inconsistent answers from the patient. The confrontation test, light reflex, funduscopy, Humphrey visual test, OCT, and MRI were normal. Malingering was suspected and a psychiatric consultation was made. The patient was found to be a victim of bullying and had a history of visual hallucinations. The patient was then diagnosed with severe depression with psychotic signs.
 Discussion : 
 Conclusion : FVL can be suspected when there is inconsistency in the results of some clinical basic tests. Despite the association between FVL and psychological problems like depression is complicated, this condition may occur in a bidirectional relationship in which depression leads to disability or contrarily. In conclusion, diagnosing visual problems in malingering patients can be challenging. Subjective and objective tests are needed to help practitioners confirm the malingering state of the patient. Practitioners also should be aware of the underlying risk of psychological problems among persons reporting visual function loss.

Depression history modulates effects of subthalamic nucleus topography on neuropsychological outcomes of deep brain stimulation for Parkinson’s disease

Patients with psychiatric symptoms, such as depression, anxiety, and visual hallucinations, may be at increased risk for adverse effects following deep brain stimulation of the subthalamic nucleus for Parkinson’s disease, but there have been relatively few studies of associations between locations of chronic stimulation and neuropsychological outcomes. We sought to determine whether psychiatric history modulates associations between stimulation location within the subthalamic nucleus and postoperative affective and cognitive changes. We retrospectively identified 42 patients with Parkinson’s disease who received bilateral subthalamic nucleus deep brain stimulation and who completed both pre- and postoperative neuropsychological testing. Active stimulation contacts were localized in MNI space using Lead-DBS software. Linear discriminant analysis identified vectors maximizing variance in postoperative neuropsychological changes, and Pearson’s correlations were used to assess for linear relationships. Stimulation location was associated with postoperative change for only 3 of the 18 neuropsychological measures. Variation along the superioinferior (z) axis was most influential. Constraining the analysis to patients with a history of depression revealed 10 measures significantly associated with active contact location, primarily related to location along the anterioposterior (y) axis and with worse outcomes associated with more anterior stimulation. Analysis of patients with a history of anxiety revealed 5 measures with location-associated changes without a predominant axis. History of visual hallucinations was not associated with significant findings. Our results suggest that a history of depression may influence the relationship between active contact location and neuropsychological outcomes following subthalamic nucleus deep brain stimulation. These patients may be more sensitive to off-target (nonmotor) stimulation.

HEIDENHAIN VARIANT OF CREUTZFELDT-JAKOB DISEASE IN BRAZIL: A CASE REPORT

Creutzfeldt-Jakob disease (CJD) is a rare spongiform encephalopathy characterized by a rapid neurodegenerative progress, caused by a misfolded variant of the cellular prion protein (PrP) known as PrPSc. The clinical presentation of sCJD includes a wide range of neurological signs of cortical, subcortical, or cerebellar origin, either isolated or in various combinations. Due to this protean clinical presentation form, sCJD must be distinguished from other dementias. In this case report, we discuss the Heidenhain variant of Creutzfeldt-Jakob disease (HvCJD), a rare variant characterized by early visual symptoms and typical findings in imaging scans. Our patient presented rapidly progressive dementia and a history of visual hallucinations. As for other prion diseases, only symptomatic treatment is available for HvCJD. Thirty years of clinical investigation of patients with prion disease have resulted in little progress in either defining or evaluating potential treatments.

Eye-related visual hallucinations: Consider ′Charles Bonnet syndrome′

The Charles Bonnet Syndrome (CBS) is typically characterized by visual hallucinations in elderly people without cognitive defects. This article presents the case of an 80-year-old male patient with a one-year history of visual hallucinations, secondary to glaucoma, in both eyes. Neither a dopamine agonist nor cholinesterase inhibitor therapy improved his symptoms. In this case, the hallucinations were gradually improved after administration of a GABAergic drug, pregabalin, for diabetic polyneuropathy. Placebo-controlled clinical trials would be needed to support this effect of pregabalin, as suggested by this association.

Mesopontine cholinergic neuron involvement in Lewy body dementia and multiple system atrophy

The pedunculopontine (PPT) and laterodorsal (LDT) tegmental nuclei are involved in control of REM sleep and thalamocortical arousal. REM sleep behavior disorder (RBD) is a feature of multiple system atrophy (MSA) and dementia with Lewy bodies (DLB), which is also associated with visual hallucinations and cognitive fluctuations. We sought to determine the degree of PPT/LDT involvement in DLB compared to MSA. We counted the cholinergic neurons in the PPT and LDT in 13 patients with neuropathologically confirmed DLB, 11 patients with MSA, and 11 control cases. Five patients with DLB and eight patients with MSA had history or polysomnographic evidence of RBD. Ten patients with DLB and no patient with MSA had history of visual hallucinations or cognitive fluctuations. There was a significant loss of PPT and LDT neurons in both DLB and MSA. Cell loss in both the PPT and LDT was more severe in MSA than in DLB. The number of cells/section for the PPT were 148 +/- 21 in controls, 54 +/- 10 in DLB (p < 0.001), and 20 +/- 3 in MSA (p < 0.001), and for the LDT, 112 +/- 16 in controls, 49 +/- 8 in DLB (p < 0.01), and 16 +/- 2 in MSA (p < 0.001). Severity of neuronal loss in MSA or DLB did not relate to the presence or absence of history of RBD. Loss of cholinergic pedunculopontine tegmental nuclei/laterodorsal tegmental nuclei neurons occurs in both dementia with Lewy bodies and multiple system atrophy but is probably not the primary mechanism of REM sleep behavior disorder in these disorders.

Disruption of White Matter Integrity in the Inferior Longitudinal Fasciculus in Adolescents With Schizophrenia as Revealed by Fiber Tractography

There is increasing evidence that schizophrenia is characterized by abnormalities in white matter. To investigate the integrity of white matter tracts in adolescents with schizophrenia. Cross-sectional, case-control, whole-brain, voxel-based analysis and fiber tractography using diffusion tensor magnetic resonance imaging. University research institute. Forty-four individuals (age range, 11-18 years), 23 with a DSM-IV diagnosis of schizophrenia or schizoaffective disorder and 21 demographically similar healthy controls. Fractional anisotropy, trace, and radial diffusivity of diffusion tensor and quantitative tractography. Voxelwise analysis revealed that adolescents with schizophrenia had reduced fractional anisotropy within the left inferior temporal (P < .001) and occipital (P < .001) regions. Tractography was performed to extract the left and the right inferior longitudinal fasciculi (ILF). Measuring the mean diffusion indices along the left ILF, patients had significantly reduced fractional anisotropy (P < .001) as well as significantly increased radial diffusivity (P < .001) and trace (P = .003) after adjusting for differences in a measure thought to reflect premorbid intelligence, Wide Range Achievement Test 3 reading scores. Exploratory analyses revealed that patients with a history of visual hallucinations had lower fractional anisotropy in the left ILF (P = .02) than patients without visual hallucinations. Our findings, which benefited from greater image resolution and methodological control than previous studies conducted in adolescents with schizophrenia, provide strong evidence for lower white matter integrity in the left ILF, particularly for patients with a history of visual hallucinations.

Cognitive Changes in Parkinson’s Disease Patients with Visual Hallucinations

Objective: To evaluate the decline in specific neuropsychological functions in nondemented Parkinson’s disease (PD) patients with a history of visual hallucinations (VH). Methods: Twenty PD patients with VH, 20 PD patients without VH and 18 normal controls were followed up over a 1-year period and assessed for cognitive decline. Results: Forty-five percent of nondemented hallucinating PD patients developed dementia during the 1-year period between baseline and follow-up evaluations. Of the nondemented hallucinating PD patients nearly 70% showed impairment in multiple cognitive domains. The progressive decline in hallucinating PD patients affected mainly visual memory for faces and visuoperceptive-visuospatial functions. Conclusion: Our results support a fast impairment of complex visual functions in hallucinating PD patients, but also a progressive decline in multiple cognitive domains, which have been identified as a risk of developing dementia in PD.

The occipital white matter lesions in Alzheimer's disease patients with visual hallucinations

Investigators have suggested that lesions responsible for visual hallucinations (VHs) are situated in the visual association cortex. The aim of this study was to assess the relationship between occipital white matter lesions and VHs in Alzheimer's disease (AD) patients. AD patients with a history of VHs (AD+VH) and those without (AD-VH) were retrospectively studied. The two groups of patients were matched by sex and mental state. All subjects underwent brain magnetic resonance image (MRI) scans. The periventricular hyperintensities (PVHs) and deep white matter hyperintensities (DWHs) on MRIs were rated by two raters using a semiquantitative scoring method (0=absent; 6=confluent). Five AD+VH patients and five AD-VH patients were enrolled into this study. The occipital PVH score was higher in the AD+VH patients than in the AD-VH patients. The occipital DWH score was zero in both groups. The presence of VHs in AD was associated with increased occipital PVHs and an absence of occipital DWHs on brain MRIs, implying that structural lesions in the geniculocalcarine region and preserved subcortical connections with visual association areas are involved in the genesis of VHs in AD.

What best differentiates Lewy body from Alzheimer's disease in early-stage dementia?

To determine which clinical feature(s) [among visual hallucinations (VH), extrapyramidal signs (EPS) and visuospatial impairment] in the earliest stages of disease best predicted a diagnosis of dementia with Lewy bodies (DLB) at autopsy, first-visit data of 23 pathologically proven DLB and 94 Alzheimer's disease cases were compared. There were no group differences with regard to age, gender, education or global severity of dementia at presentation (mean Mini-Mental State Examination: 24.0 versus 25.0, mean Dementia Rating Scale: 123.6 versus 125.7). DLB patients at initial presentation displayed an increased frequency of VH (P = 0.001), but not EPS (P = 0.3), compared to Alzheimer's disease patients. However, only a minority of DLB cases had either VH (22%), EPS (26%) or both (13%). In contrast, although not a core feature, visuospatial/constructional impairment was observed in most of the DLB cases (74%). Among clinical variables, presence/recent history of VH was the most specific to DLB (99%), and visuospatial impairment was the most sensitive (74%). As a result, VH at presentation were the best positive predictor of DLB at autopsy (positive predictive value: 83% versus 32% or less for all other variables), while lack of visuospatial impairment was the best negative predictor (negative predictive value: 90%). We conclude that the best model for differentiating DLB from Alzheimer's disease in the earliest stages of disease includes VH and visuospatial/constructional dysfunction, but not spontaneous EPS, as predictors. This suggests that clinical history plus a brief assessment of visuospatial function may be of the greatest value in correctly identifying DLB early during the course of disease.

Olanzapine therapy in hallucinatory visions related to Bonnet syndrome

Charles Bonnet syndrome (CBS) is characterised by the triad of complex visual hallucinations, ocular pathology causing visual deterioration and preserved cognitive status. We report a case of a 62-year-old man with a brief history of visual hallucinations. The patient complained of amaurosis with optic nerve atrophy in his left eye and a severe impairment of visual acuity in the right and suddenly experienced complex, vivid, elaborate and coloured visual hallucinations persisting long after eye closure and stopping during sleep. The patient maintained his insight, criticising these visions as unreal and felt distressed by them. Hallucination onset was 3 days before hospital admission. No cognitive impairment and no diseases apart from prostatic adenoma treated with alpha-lythic therapy were reported. Neurological examination and neuroimaging data were normal. Therapy with olanzapine (OLZ) 5 mg/day led to a progressive clearance of visual hallucinations in seven days and was gradually reduced and withdrawn. Three months later the visions reappeared and OLZ 5 mg/day yielded a persisting remission so that at the follow-up examination after 1 year on therapy the patient is still asymptomatic. To date, no established treatment for CBS is stated and in some patients the hallucinations fade spontaneously; in our case an antipsychotic therapy with OLZ was effective while generally anticonvulsant drugs with different mechanism of action such as carbamazepine, valproate and gabapentin are proposed.

Visual hallucinations, white matter lesions and disease severity in Parkinson's disease.

To determine if visual hallucinations in patients with Parkinson's disease are associated with an increased prevalence of white matter lesions. Fifteen patients with (group 1) and 15 patients without (group 2) a history of visual hallucinations were studied. Both groups were matched for age. Magnetic resonance imaging was performed in all patients using standard T2 weighted Fast-Spin-Echo sequences. Assessment of cerebral white matter changes was performed using a modification of established criteria, with semiquantitative evaluation of periventricular and deep white matter changes. There was no significant group difference with regard to the total amount of white matter changes, nor was a group difference found between the amount or extent of periventricular hyperintensities or deep white matter lesions. Group 1 was significantly (P = 0.001) more disabled as evaluated by Hoehn/Yahr stage controlling for age and duration of disease. Mean increases in Hoehn/Yahr stage were not significantly greater in group 1 compared with group 2 at a 2-year follow-up examination (0.6 vs. 0.3, P = 0.166). Our data suggest that visual hallucinations are an indicator of a more aggressive course of the disease, but are not associated with a higher prevalence of global or occipital white matter lesions.

Possible allelic association of a tyrosine hydroxylase polymorphism with vulnerability to alcohol-withdrawal delirium.

Recently, an association has been reported between schizophrenia and a rare allele containing 10-repeats (A10) of a polymorphic tetranucleotide motif in the first intron of the tyrosine hydroxylase (TH) gene. The present association analysis tested the hypothesis that the A10 candidate allele confers vulnerability to alcohol-withdrawal delirium with visual hallucinations. The genotype of the TH tetranucleotide polymorphism was assessed in 204 German controls and 311 German alcohol-dependent subjects, including 63 alcoholics with a history of visual hallucinations during withdrawal delirium. The frequency of the A10 allele was significantly increased in the alcoholics with withdrawal delirium (3.2%) compared with that in the controls (0.5%; Fisher's exact test: P = 0.03, two-tailed; OR (A10+) = 6.85, 95% confidence interval: 1.52-30.79). The possible allelic association suggests that allelic variation at the TH locus mediates vulnerability to alcohol-withdrawal delirium in a small proportion of alcohol-dependent subjects.

Charles Bonnet Syndrome in a Centenarian

To the Editor. —Charles Bonnet syndrome (CBS) includes visual pseudohallucinations (hallucinations with preserved insight), visual deprivation, and preserved cognitive status.1We present a patient who improved without medications. Report of a Case. —A 103-year-old widow presented with a 1-year history of visual hallucinations, which she recognized as unreal. They appeared during the day and disappeared when she closed her eyes. The visions were related to past experiences, such as when she was a child or a teacher, and were often pleasant. She was previously treated with phenothiazines, but without effect. She had glaucoma of the right eye and a cataract in the left eye. She had decreased visual acuity (OD 20/200, OS 20/100). Results of her neurological examination, cognitive status, Geriatric Depression Scale, and computed tomographic scan were normal. Increasing communication and occupational therapy decreased the frequency of the visions. Comment. —The diagnosis of CBS is by exclusion of