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Looking forward to the many coming releases this year". These sensory distortions range from the shimmering zigzags of a visual migraine to powerful visions brought on by fever, injuries, drugs, sensory deprivation, exhaustion, or even grief. Hallucinations doubtless lie behind many mythological traditions, literary inventions, and religious epiphanies. Drawing on his own experiences, a wealth of clinical cases from among his patients, and famous historical examples ranging from Dostoevsky to Lewis Carroll, the legendary neurologist Oliver Sacks investigates the mystery of these sensory deceptions: what they say about the working of our brains, how they have influenced our folklore and culture, and why the potential for hallucination is present in us all.
Score: 4. With its arbitrary yet determinant alphabetical arrangement, its gleeful pursuit of the ludic pleasure of word games acrostic, anagram, homophone, parody, pun , as well as its reflections on the politics of language and dialect, Mullen's work is serious play.
This method of textual transformation--which is used to compose nonsensical travesties reminiscent of Lewis Carroll's "Jabberwocky"--also creates a kind of automatic poetic discourse. Mullen's parodies reconceive the African American's relation to the English language and Anglophone writing, through textual reproduction, recombining the genetic structure of texts from the Shakespearean sonnet and the fairy tale to airline safety instructions and unsolicited mail.
The poet admits to being "licked all over by the English tongue," and the title of this book may remind readers that an intimate partner who also gives language lessons is called, euphemistically, a "pillow dictionary.
A Dictionary of Neurological Signs seeks to elucidate the interpretation of neurological signs "neurosemiology" : their anatomical, physiological, and pathological significance. Each entry includes: definition of the sign; brief account of the clinical technique required to elicit the sign; description of the other signs which may accompany the index sign. The Dictionary provides practical, concise answers to complex clinical questions. It will consist of 28 chapters, the writing of which will be put out to international experts specialized in the specific fields at hand.
The work aims to be unique, in that it intends to cover many different types of hallucination, and to approach the subject matter from four different perspectives, i. Hansebooks is editor of the literature on different topic areas such as research and science, travel and expeditions, cooking and nutrition, medicine, and other genres. As a publisher we focus on the preservation of historical literature.
Many works of historical writers and scientists are available today as antiques only. Hansebooks newly publishes these books and contributes to the preservation of literature which has become rare and historical knowledge for the future. Like those editions, this Third Edition, updated and expanded, can be almost as well described in terms of what the book is not, along with details about what it is. The Dictionary is not a handbook for treatment of neurological disorders.
While many entries provide the latest treatment options, up-to-the-minute therapies are not discussed in bedside level detail. The Dictionary is an alphabetical listing of commonly presenting neurological signs designed to guide the physician toward the correct clinical diagnosis.
The Dictionary is focused, problem-based, concise and practical. The structured entries in this practical, clinical resource provide a thumbnail of a wide range of neurological signs. The Dictionary of Neurological Signs, Third Edition, is an indispensable reference for all students, trainees, and clinicians who care for patients with neurological disorders. Their study has become a critical aspect of our knowledge of the brain, making significant strides in recent years with advances in neuroimaging, and has established common ground among what normally are regarded as disparate fields.
The Neuroscience of Hallucinations synthesizes the most up-to-date findings on these intriguing auditory, visual, olfactory, gustatory, and somatosensory experiences, from their molecular origins to their cognitive expression. Dementia with Lewy bodies DLB is the second most common form of dementia after dementia of the Alzheimer's type. Patients may have insight into their hallucinatory content.
Visual hallucinations are an important clinical clue indicating that dementia may be associated with Lewy bodies rather than with another subtype of dementia.
Tiraboschi et al. Harding and colleagues 20 reported a strong correlation between Lewy bodies located in the temporal structures specifically in the amygdala and the parahippocampus and well-formed visual hallucinations. Visual hallucinations also occur in up to half of patients with Parkinson's disease. Posterior cortical atrophy is another neurodegenerative syndrome associated with visual hallucinations and parkinsonian symptoms.
The chief pathologic features of posterior cortical atrophy are neurofibrillary tangles and senile plaques similar to those seen in dementia of the Alzheimer's type but with a distribution limited to the occipital and parietal lobes. Patients with posterior cortical atrophy may present with visual agnosia, anomia, apraxia, and features of Gerstmann syndrome.
The Charles Bonnet syndrome CBS involves the occurrence of visual hallucinations in the visually impaired. Any cause of visual impairment including macular degeneration, glaucoma, cataracts, cerebrovascular disease, and tumors may be associated with CBS. Charles Bonnet syndrome has been thought of as a nonpsychiatric cause of visual hallucinations; while this remains true, there is growing evidence that preexisting dementia or cognitive impairment may predispose a patient to the development of CBS.
The visual hallucinations in CBS have been described as clear and detailed; they often involve people, faces, animals, and inanimate objects. While patients may initially be unaware that these images are indeed hallucinations, one of the hallmarks of CBS is the eventual development of insight regarding their visual hallucinations.
The strongest risk factors for CBS include bilateral visual impairment, declining visual acuity, cerebral damage, cognitive defects, social isolation, and sensory deprivation. Antipsychotics and selective serotonin reuptake inhibitors have been used to treat CBS, but there is no clear evidence to support this approach.
Anton's syndrome is a rare condition in which patients with cortical blindness deny that they have visual loss. This presentation has been described as a combination of anosognosia and confabulation. The problem may only be discovered when the patient is found running into or falling over objects while reporting odd or fantastical reasons why they did not see the object with which they collided.
The mechanism that underlies Anton's syndrome remains unclear, but it is thought to be related to infarction of the primary visual cortex Brodmann's area 17 with preserved function of the visual association cortices. These patients may have alterations in emotional reactivity that predispose them to denial. Another hypothesis suggests that there may be a synesthetic translation of the remaining senses into mental images that are perceived by the patient as vision.
Visual hallucinations caused by seizures have often been described as simple, brief, and consistent for each patient; they usually consist of small, brightly colored spots or shapes that flash.
Those that remain isolated in 1 visual field suggest seizure activity that originates on the contralateral side. Complex visual hallucinations due to seizures are thought to require the involvement of the visual association cortex. Since occipital seizures are frequently accompanied by a postictal headache, they may be difficult to distinguish from migraines, creating confusion and the delay of appropriate treatment.
While neurologic literature indicates that visual hallucinations associated with seizures are simple, there is a growing body of work that describes complex, formed visual hallucinations as ictal, peri-ictal, and intra-ictal phenomena.
The occurrence of complex visual hallucinations as a symptom of epilepsy can be a point of disagreement between neurologists and psychiatrists. Visual hallucinations associated with migraine headaches can be a classic aura of migraine as well as a less common manifestation such as migraine coma and familial hemiplegic migraine. Variations of this classic picture such as colored patterns also occur.
The simple visual hallucinations described above are the most common, but more complex hallucinations can occur in migraine coma and familial hemiplegic migraine. Hadjikhani and colleagues 43 used functional magnetic resonance imaging fMRI to show that migraine aura is likely caused by spreading cortical depression.
This phenomenon involves a brief period of hyperperfusion followed by a slow spreading wave of hypoperfusion. These events are thought to be due to a neuronal dysfunction rather than to a primary vascular event. Peduncular hallucinosis is characterized by visual hallucinations that arise following an infarct of the midbrain. It was originally described in by Lhermitte and has since been the topic of many case reports.
The mechanism has been difficult to pinpoint since the literature features a wide variety of lesions. Lesions may involve the cerebral peduncles, but most often involve the reticular formation or its targets. Each hallucination may last from minutes to hours, often occurring in the evening.
Patients eventually develop insight into their hallucinations, and they may find them interesting or amusing. Hypnagogic hallucinations are visual and auditory perceptions that occur during sleep onset, while hypnopompic hallucinations occur on awakening. They are usually visual and may be bizarre and dreamlike, but with some preservation of consciousness.
It was also shown that patients with insomnia, excessive daytime sleepiness, or mental disorders were more likely to experience hallucinations.
Many drugs are labeled as hallucinogens because they alter perceptions, 48 although true hallucinations are perceptions in the absence of any actual stimulus. Hallucinogenic drugs including mescaline, psilocybin, and lysergic acid diethylamide [LSD] are agonists of serotonin 5-HT 2A receptors; they do not always produce true hallucinations unless they are used at high doses.
The effects also depend to some degree on the mood of the user and the situation in which the drug is used. Other drugs often considered to be hallucinogenic include phencyclidine PCP , ecstasy, atropine, and dopamine agonists.
Tumors that lie along, or compress, the optic path may cause visual hallucinations. In one case series, 13 of 59 patients with temporal lobe tumors experienced visual hallucinations.
The majority of these visual hallucinations are thought to be related to seizure activity caused by the tumor. A handful of inborn errors of metabolism may cause visual hallucinations. While these are quite rare, they are nonetheless important to consider because patients with inborn errors of metabolism may present with hallucinations at a time when their disease is treatable and when serious neurologic damage has not yet occurred. Creutzfeldt-Jakob disease CJD is a fatal progressive neurodegenerative illness caused by central nervous system prion infection.
Symptoms of CJD may also include visual hallucinations, especially in the Heidenhain variant of the illness.
Visual effects may include color changes, visual field defects, visual agnosia, cortical blindness, metamorphopsia, and micropsia that progresses to the frank visual hallucinations characteristic of the Heidenhain variant.
Given the broad variety of potential etiologies of visual hallucinations outlined previously, it is clear that an accurate diagnosis is required before effective treatment can be initiated. A thorough history and clinical examination are the most vital elements of a workup for visual hallucinations. Associated symptoms and characteristics of the visual hallucinations themselves may help direct diagnosis Table 1.
The elicitation of signs or symptoms of psychosis, inattention, parkinsonism, impaired vision, or headache will narrow the diagnosis and prompt further diagnostic studies. An EEG is potentially the most revealing diagnostic study, since it can not only highlight seizure activity, but also detect delirium with theta-delta slowing , delirium tremens with rapid beta activity , and CJD with occipital periodic non-generalizing complexes.
Since effective treatment of visual hallucinations see Table 2 is entirely dependent on the underlying cause, care should be taken to ensure diagnostic accuracy, especially since treatments that may be beneficial for one cause of visual hallucinations may exacerbate another.
For example, benzodiazepines are the treatment of choice for delirium tremens, but they will almost certainly worsen a delirium due to any other cause. Neuroleptic medications i. These medications are also beneficial for the management of delirium in which hallucinations are thought to be due to release of endogenous dopamine , with intravenous haloperidol having the most evidence for safety and efficacy.
Unfortunately, due to their dopamine-blocking activity, most neuroleptics will significantly exacerbate parkinsonian symptoms in patients with DLB or dementia associated with Parkinson's disease. Quetiapine and clozapine have a niche role in the treatment of these patients, since their very low affinity for dopamine receptors renders them less likely to cause this serious adverse effect.
More focal causes of visual hallucinations may require more focal treatment. Unfortunately, some causes of visual hallucinations e. For these patients, neuroleptics may minimize visual hallucinations and distress. Most patients with visual hallucinations, regardless of cause, will benefit from the reassurance of their caregivers.
Some may also benefit from more formal psychotherapeutic interventions e. Lessons Learned at the Interface of Medicine and Psychiatry. Such consultations require the integration of medical and psychiatric knowledge.
During their thrice-weekly rounds, Dr. Stern and other members of the Psychiatric Consultation Service discuss the diagnosis and management of conditions confronted. These discussions have given rise to rounds reports that will prove useful for clinicians practicing at the interface of medicine and psychiatry.
Teeple is a fourth-year medical student at the University of Arizona College of Medicine. Stern is chief of the psychiatric consultation service at MGH and a professor of psychiatry at Harvard Medical School. The authors report no sources of financial or material support for this article. Teeple and Dr. Caplan report no conflict of interest relating to this article.
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