Complex Visual Disturbances Research Articles

Complex visual hallucinations in a patient with chronic schizophrenia and alcohol dependence: a case report and literature review

AbstractThe aim of this study was to report a patient with complex visual perceptual disturbances and a 30-year history of schizophrenia and alcohol dependence, and to formulate a comprehensive clinical approach to this unique neuropsychiatric phenomenon.The authors report subjective and objective information from the patient’s past medial history and current admission. The authors also did a comprehensive review of the literature on complex visual hallucinations.Complex visual hallucination is a frightening experience, with a pathogenesis ranging from chronic psychiatric disorders, such as schizophrenia, to acute neurological events, such as cerebrovascular accident. The hallucination content is typically described by patients as vivid with dynamic images, in striking colors and clear contours. The authors report a patient earlier diagnosed with schizophrenia and alcohol dependence disorder who became agitated following a sudden onset of visions of vivid, interactive images of people and animals.Due to the scope of the differential diagnosis, identifying the exact underlying etiology of complex visual hallucinations is often challenging, yet critical, in preventing the high risk of morbidity and mortality associated with some of the root causes of this neuropsychiatric phenomenon.

Functional neurological disorders in children and young people

Neurology and psychiatry are closely intertwined, nowhere more so than in the realm of non-organic functional disorders of the nervous system, which constitute 2–10% of patients seen in paediatric clinics.1 Often the patient has seen several doctors – none committing to a firm diagnosis of non-organic disorder despite suspicions. Parents are often reluctant to consider psychological factors, or to seek help from child and adolescent mental health professionals because of a perceived stigma and possible self-blame. Freud viewed hysterical symptoms as the transformation of inner psychological conflict into physical symptoms by displacement. Current psychiatric terminology distinguishes two types of disorder (DSM IV-TR) previously labelled ‘hysteria’: somatoform and dissociative. The former includes conversion, somatization, pain disorders, hypochondriasis, and body dysmorphic disorders. The latter includes dissociative amnesia and fugue. Often there is comorbid mood and anxiety disorder1-3 and discussion of their origins may prove a fruitful line of enquiry. The presence of high levels of childhood trauma retrospectively reported by adult sufferers2 has led some to view these disorders as a post-traumatic response, especially among genetically predisposed individuals.4 Functional neurological disorders are usually seen in adolescents (twofold more common in females) and occur across a range of cognitive ability. Symptoms may follow minor illness, injury, and in rare instances, abuse.1, 2, 4 Presenting symptoms and signs include non-epileptic seizures (often on a background of mild epilepsy), paralysis, gait disorders, complex pain syndromes, bizarre sensory and visual disturbances, and chronic fatigue.1 Affected patients have often stopped attending school, losing both educational opportunity and the social stimulation provided by peers. This inevitably causes functional deterioration, social isolation, and subsequent reintegration challenges. Patients may derive subtle and not so subtle secondary gains; e.g. getting parental attention and not having to face up to a challenging situation. However, malingering is rare.1 Clinical examination is normal or inconsistently abnormal. Careful medical and nursing observation over time often highlights incongruities. Neurological disorders that rarely present with psychiatric features (e.g. Wilson disease, systemic lupus erythematosus, NMDA receptor antibody mediated encephalitis) need exclusion. Usually, investigations are normal or show minor ambiguities. Physical illness specialists must conduct thorough investigations quickly and draw a line under them in order not to over-medicalize and entrench the problem. Engagement with patient and family in a non-judgemental, empathetic way is helpful. The doctor should acknowledge that there is a problem, despite not having found a physical cause to explain it. The diagnosis must be explained in an honest, logical, and inoffensive manner. A positive emphasis is placed on the apparently baffling normality of tests, indicating no damage to the hardware of the nervous system, but a temporary and reversible malfunction in its software.5 The doctor states to the young person the need for a balance of physical and emotional well-being to function as a ‘whole’. The family are counselled to shift focus from causation to treatment. The patient and family are best served by a multidisciplinary team including paediatric neurologists and experienced nursing, physiotherapy, and adolescent mental health professionals, providing a consistent coordinated care plan to improve function using physical and psychological strategies. The value of child mental health colleagues can be compared with ‘motivators’ used by sports celebrities. Comorbid depression or anxiety is treated. Cognitive behavioural therapy is often employed in the context of an overall rehabilitation philosophy. Care is taken to deal with the patient primarily on a one-to-one basis and allow for symptom resolution with dignity and without loss of face. It is known from adult literature that without timely resolution the problem becomes chronic with severe personal and economic consequences.5 In one paediatric series only 56% of patients were ‘cured’ on follow-up over 7½ years.3 The patient journey through the healthcare system is well defined for physical illness, unlike for functional disorders. I have run a successful joint clinic for over a decade (with a consultant child and adolescent psychiatrist) in a multidisciplinary format for young people with functional disorders, with excellent audited outcomes. We believe it to be a rewarding, mutually beneficial, and reassuring partnership in an often frustrating area, not least because, unlike disorders paediatric neurologists diagnose, this one is eminently treatable. The value of such a combined care model has been demonstrated previously.3

Complex Visual Manifestations of Posterior Cortical Atrophy

We describe 5 patients with complex visual disturbances in the absence of ocular pathology who were ultimately diagnosed with posterior cortical atrophy (PCA). The presence of visual cortical symptoms, neuroimaging findings and clinical evolution led to the diagnosis 1-5 years after the onset of visual symptoms. Age of onset ranged from 50-66 years. In 3 cases, magnetic resonance imaging (MRI) of the brain demonstrated predominantly right posterior cortical atrophy. The other 2 patients had nonspecific MRI findings but the diagnosis was established given the findings on clinical examination and positron emission tomography (PET). All progressed to global dementia and an autopsy confirmed the diagnosis of Alzheimer disease in one patient. The possibility of PCA should be considered when a patient presents with complex visual symptoms in the absence of ocular pathology. Early neurological assessment may avoid diagnostic delay.

Complex visual disturbances during maprotiline treatment

ALTHOUGH MAPROTILINE IS no longer a first-choice agent for treating major depression, it is sometimes used in combination with a selective serotonin re-uptake inhibitor in treatment-resistant depression. Here, we report the case of a woman who developed complex visual disturbances after maprotiline use. At the age of 63, the patient began to experience depression and was treated at Jichi Medical University Hospital. At that time, the medication did not have any effect, and she underwent electroconvulsive therapy, which proved effective. The patient was readmitted at the age of 64 because depression recurred. At the time of admission, her medication history was as follows: milnacipran, trazodone, and amitriptyline. After the admission, she was prescribed only trazodone 150 mg/day. Because no marked improvement was observed, maprotiline was given at 25 mg/day, and the dose was increased up to 100 mg/day. Maprotiline at a dose of 75 mg triggered pareidolia (‘seeing shadows looking like someone's face’), visual hallucination (‘seeing faces of people and animals in the mirror’), and visual disturbance (‘feeling that floors and walls are approaching’). The patient was aware that these experiences were not real images. Because they appeared after maprotiline use, the complex visual disturbances were suspected to be a side-effect of maprotiline. Therefore, maprotiline was reduced and then was discontinued, following which the symptoms disappeared. Magnetic resonance imaging, single-photon-emission computed tomography, and electroencephalography were normal. Hori et al. reported a case of symptoms of visual perseveration induced by maprotiline.1 The present patient experienced pareidolia, visual hallucination, and visual disturbance. The symptoms reported in both cases were not exactly the same, but the present case is the second report of visual disturbances induced by maprotiline. Some authors have put forward hypotheses to explain the mechanisms underlying maprotiline-induced visual impairment. The symptoms in the Hori et al. report were thought to be caused by the anticholinergic effect of maprotiline. Maprotiline is thought to be a noradrenaline re-uptake inhibitor, whereas hallucinations result from an increase in dopamine levels. Kihara and Ikeda found an increase in dopamine levels due to maprotiline.2 Their findings were consistent with those of Carboni et al., who stated that the increase in dopamine levels was caused by a carrier of the noradrenaline uptake inhibitor.3 The complex visual disturbances in the present case may have been associated with maprotiline-induced increase in dopamine levels or an anticholinergic effect. Nevertheless, visual impairment is a rare side-effect of antidepressants, and physicians should be aware of this rare phenomenon.

Hallucinogen-persisting perception disorder

A 33-year-old female patient developed a hallucinogen-persisting perception disorder (HPPD) after lysergic acid diethylamide (LSD) abuse for a year at the age of 18. Specifically, she reported after images, perception of movement in her peripheral visual fields, blurring of small patterns, halo effects, and macro- and micropsia. Previous treatment with antidepressants and risperidone failed to ameliorate these symptoms. Upon commencing drug therapy with lamotrigine, these complex visual disturbances receded almost completely. Based on its hypothesized neuroprotective and mood-stabilizing effects, the antiepileptic lamotrigine may offer a promising new approach in the treatment of HPPD.

WALLENBERG'S SYNDROME

A consecutive series of 10 typical and 4 partial cases of Wallenberg's syndrome is presented. The most prominent symptoms in these patients were found to be imbalance and various complex visual disturbances showing a rather distinct pattern characterized by tilt of the surroundings, oblique diplopia, difficulties of fixation and visual blurring. LateropuIsion was in all cases more or less clearly directed towards the side of the infarction. Imbalance, lateropulsion and visual disturbances as a rule improved rapidly but persisting disability was due to these features.

Isolated numerical skills in posterior cortical atrophy—An fMRI study

Posterior cortical atrophy (PCA) is characterized by bilateral parieto-occipito-temporal atrophy and hypometabolism. Neuropsychological impairments include complex visual disturbances, alexia, agraphia, finger agnosia, right–left disorientation and dyscalculia. A recent case study reported severe numerical deficits with some selectively preserved numerical skills in a patient affected by PCA [Delazer, M., Karner, E., Zamarian, L., Donnemiller, E., & Benke, T. (2006). Number processing in posterior cortical atrophy—a neuropsycholgical case study. Neuropsychologia]. In a functional magnetic resonance imaging (fMRI) study brain activation patterns related to these selectively preserved numerical skills were analyzed. Recitation of multiplication tables and counting forward were contrasted to word recitation in a block design. Contrasts between experimental conditions and control condition yielded significant activation of inferior and medial temporal structures. Since numerical processing is generally associated with parietal activation, it was hypothesized that preserved brain structures would compensate for the functional deficits.

Uncommon neurodegenerative causes of dementia

A group of neurodegenerative diseases is outlined that affect cortical and subcortical areas of the brain. These diseases give rise to atypical forms of dementia and, unlike Alzheimer's disease (AD), are often associated with neurological symptoms. Clinical symptoms reflect the localization of the degenerative process rather than the nature of the underlying histopathology. Degeneration of the frontal and anterior temporal lobe presents initially with behavioral alterations, but later in the course, impairment of cognition and activities of daily living develops. Posterior cortical atrophy affects the parietal and occipital association cortices and causes complex visual disturbances. In corticobasal degeneration (CBD) the focus of pathology includes the frontoparietal cortex and several subcortical nuclei, causing symmetrical rigidity, bradykinesia, myoclonus and dystonia. Progressive supranuclear palsy (PSP) involves the frontal, temporal and parietal cortex as well as parts of the brain stem. Clinical features include a hypokinetic rigid syndrome with nuchal dystonia and vertical gaze palsy. Huntington's disease is a prototypical autosomal dominant disorder that affects the extrapyramidal system and causes choreatic movements in combination with personality changes and cognitive deterioration. Amyotrophic lateral sclerosis (ALS) with dementia is a neurodegeneration of the frontotemporal cortex and of the anterior horn of the spinal cord. Behavioral change similar to frontotemporal dementia (FTD) is paralleled or followed by the classic features of motor neuron disease.

Clinical assessment of complex visual dysfunction.

The study of patients with lesions of the central visual system has shown that certain complex visual disturbances are generally associated with lesions in the ventral occipital lobe and adjoining temporal lobe, while other disturbances are more commonly associated with lesions of the dorsal occipital cortices and adjoining parietal lobe. Cerebrovascular lesions in the distribution of the posterior cerebral artery, tumor, trauma, and neurodegenerative processes such as Alzheimer's disease are common etiologies of these disturbances and can be assessed using modern neuroimaging techniques. The corresponding visual function deficits can be separated out by a systematic clinical approach incorporating visual sensory and cognitive testing procedures, as outlined below.

Complex visual disturbances in Alzheimer's disease

Although Alzheimer's disease (AD) involves visual association cortex, previous studies have not systematically investigated complex visual disturbances in AD. We examined 30 community-based AD patients, 13 (43%) of whom had complex visual complaints, and compared them with 30 controls on 7 types of complex visual tasks. Despite preserved visual acuity and color recognition, the AD patients were impaired in the visual evaluation of common objects, famous faces, spatial locations, and complex figures. In the AD patients, we found that all 30 had disturbances in figure-ground analysis; 17 (57%) had difficulties visually recognizing actual objects ("agnosia"); those with worse dementia disability had the most complex visual disturbances; and a subgroup (6) with Balint's syndrome performed the most poorly on the complex visual tasks. This study demonstrates that a range of complex visual disturbances are common in AD and suggests that they may result from the known neuropathology in the visual association cortex.

Migraine-like accompaniments of vitreous detachment

Vitreous detachment is occasionally associated with complex visual disturbances and/or cephalgia, not just flashes and floaters. The author analyzes his experience with unusual symptoms described by patients suffering acute vitreous detachment and concludes that many of them resemble symptoms experienced by migraineurs. He reviews experimental models of migraine in the context of retinal neuronal spreading depression and speculates that electrical disturbances of the retina may be related to a variety of visual symptoms of an acute or subacute nature.

Experiments on the Production of an Imitation of Sea Sickness by Complex Visual Disturbances

Experiments on the Production of an Imitation of Sea Sickness by Complex Visual Disturbances