© Borgis - New Medicine 2/2002, s. 83-88
Andrzej Brzecki, Krystyna Kobel-Buys, Guido Buys
Hallucinations, illusions, and other visual distrubances in neurology
The Center of Rehabilitation for Children and Adults, Mikoszów (Strzelin), Poland
The authors describe the visual pathway and especially the posterior part of the optic visual radiation and visual representation in the cuneus of the occipital cortex. Almost the entire visual tract is supplied by the posterior cerebral artery, except for central vision representation, which is supplied by a branch of the middle cerebral artery. Therefore, damage to the visual pathway of one hemisphere may cause heteronymous hemianopsia or quadrantanopsia and, less frequently, visual hallucinations and illusions.
Hallucinations and illusions may also occur – exempli gratia – in infectious encephalopathies, poisonings, sleep disorders and psychoses. In particular, stimulation of the temporal lobe by toxins or drugs having dopaminergic, serotoninergic or adrenergic actions (frequently true or „false” neurotransmitters) may also cause them.
Examples of paintings done by artist under the influence of some hallucinogens has been presented. Prosopgnosia and prosopagnosia have been discussed. Prosopagnosia may be caused by an injury the right hemisphere. Anosognosia of the left part of the body and the left visual field have to been also discussed.
A case study of a patient with visual hallucinations and illusions of his own enormous extremities in the course of thrombosis of the posterior cerebral artery has been mentioned. Also, in connection with this theme, we discussed anosognosia of the left part of the body and left visual field spatial neglect, cortical blindness etc. and we mentioned border zone infarcts as a new problem of vascular diseases in elderly patients.
Clinical examples of hypnagogic hallucinations occurring in sleep deprivation and in narcolepsy have been presented.
The problem of different kinds of hallucinations and their relation to the ability to draw or paint in patients with schizophrenia have been discussed and illustrated.
The visual tracts start in the retina, and through the optic nerve, optic chiasma, and optic tract lead to the primary visual centres, to the lateral geniculate body. This has a similar structure to that which is found in the visual cortex, which is why, it is surmised, it has a specific significance in visual perception. Finally, the visual tract reaches the pulvinar and the superior colliculus, and the pretectal area.
The visual tract is later prolonged as the optic radiation, from the ventricular triangle, as the posterior part of the optic radiation splits and runs above and below the calcarine fissure (42). A lesion of the optic radiation, located before the connection with the primary visual cortex, causes superior and inferior quadrantic hemianopsia. Damage to the primary visual cortex (caused by hypoxia, trauma, or tumour, Alzheimer´s degeneration and others) is a cause of cortical blindness, with preserved central vision (macular and fixational), and sometimes with Anton´s syndrome – i.e.: a denial of having cortical blindness. Poor unilateral or bilateral vision may be accompanied by hallucinations and illusions.
The primary or striated visual cortex, called V1 in neurophysiological terms, is supplied by the posterior artery of the brain. This excludes the posterior part, which handles central field vision, and is supplied by a branch of the middle artery (36, 45). The primary visual cortex is surrounded by fields V2, V3, and V4, the medial region of the temporal-occipital region, which is probably responsible for perception of colour and shape (55). An injury to this area causes colour agnosia.
Field V5 in the vicinity of the angular gyrus, and, together with part of the optic radiation, is probably supplied by a branch of the middle brain artery. This field has a special significance in movement perception within the visual field, which continues to operate even after an injury to the primary visual cortex (56). This was demonstrated by Riddoch in 1917 (44).
Descending tracts from the visual cortical centres are parallel to the ascending tracts (24), and serve to control visual stimulation, by feedback. Other descending tracts run to the parietal and temporal lobes, and determine the conscious process of vision as a separate cortical visual pathways, one which is specialised for spatial perception (where an object is) and follows a dorsal route from the occipital to the parietal lobes and the other which is specialised for specifying what an object is and follows a route from the occipital to temporal lobes (54).
Therefore, cutting the descending impulses from the visual cortex may cause a composite agnosia of the face (prosopagnosia), colour vision agnosia, alexia, achromatopsy (colour vision agnosia, or seeing black-and-white objects in colours), and simultant agnosia. In the same way as the ascending tracts, injury may lead to hallucinations and illusions.
Illusions are defined as deformations of normal image: these include metamorphoses (elongation or distortion which may cause, for example seeing a head in a grotesque way, or seeing a picture which is placed in an inappropriate field of vision), micropsy, macropsy, teleopsy (seeing objects from a certain distance), poliopsy, allesthesia (seeing objects in another part of the visual field, which means seeing the object in two different places), polynopsia (overlapping of recently-seen objects on a current image, or perseverance) (9, 33).
Simple and composite hallucinations may be defined as seeing unreal shapes, objects, animals, human beings, or fantastic creatures. The phenomena occur in 10% of cases of amblyopia (hemianopsia) caused by a stroke (28).
In cases of infectious or metabolic encephalopathies, drug abuse, psychoses, sleep disorders, hallucinations and illusions probably occur because of lack of light stimulation, sleep deprivation, and/or cerebral cortex stimulation, caused by real or "false” neurotransmitters (40).
Hallucinations and illusions may occur together with other occipital, temporal, and parietal disturbances (olfactory, gustatory, and other hallucinations). In vascular injury to the posterior region of the optic radiation and visual cortex (which is usually caused by thrombosis or embolus), there is occasional hypotension – this results in insufficient cerebral blood perfusion in the regions supplied by the posterior, anterior or middle brain artery (border zone infarcts) (3, 4, 7, 23, 27, 39, 50).
Less frequently, injury to the optic radiation or visual cortex is caused by arterial hypertension, rupture of an aneurysm, various blood diseases, antithrombotic drugs, haemorrhagic inflammation of the brain, bleeding of a tumour, etc. Among other causes are epilepsy, tumours, brain contusion, inflammation, Creutzfeld-Jacob disease, poisoning, Alzheimer´s disease, and other diseases caused by cerebral atrophy, progressive multi-focal leucoencephalopathy, adrenoleukodystrophy in childhood, and various intoxicants, including poisoning with hallucinogens (11, 12, 26).
Hallucinations and illusions may be present in various eye conditions, retinal degeneration (1), and other eye diseases (49). They may appear in darkness, especially in elderly persons with poor eyesight (16).
Hallucinations and visual illusions are sometimes observed in the states of delirium or obnubilation, or in serious emotional disturbances in schizophrenia, in which latter hallucinations may particularly arise as a result of limited contact with the natural surroundings (53).
The symptoms arising in the primary visual cortex are simple hallucination, i.e.: scotoma, photopsy, or photoma (wavy movements, stripes, mists, and shade). Injury to the posterior part of the optic radiation and descending occipital-parietal fibres and/or occipital-temporal fibres may occasionally be the cause of hallucinations and illusions (8).
An injury of the left (dominant) angular gyrus or its adjacent regions is the cause of Gerstmann syndrome (alexia with agraphia, acalculia, the fingers agnosia, impairment of left-right side orientation), which may be bound up with quadrantic hemianopsia and visual hallucinations (10, 20).
Damage to the connections running from the V1-V3 visual cortex (of the dominant hemisphere) to the angular gyrus manifests hemianopsia and pure alexia, which is sometimes accompanied by visual agnosia and in cases of damage to the angular gyrus with alexia and agraphia.
Damage of the right parietal and temporal lobes maybe the cause of prosopagnosia i.e. inability to recognize a well-known face. The visual stimuli coming from all visual fields (V1-V5) reach mainly the right but also the left hemisphere cortex, where the elements of the face are coded and mental features bound up with them (6).
MRI studies confirm observations that the right occipital-temporal region is responsible for the recognition of the face. Inability to recognize a very well-known face may be a developmental or acquired impairment. Recognition of a face is primary in mental development of the child and enables him to differentiate the mother´s face from others.
The manifestation of "a spirit” (supreme mental functions) may be observed in the face as proud, concentration, impudence, shrewdness and many more, which a talented painter (or photographer) may present as a portrait. Face recognition (prosopgnosia) is associated with the original representation of somebody´s face and emotions, the speech pattern and other features. It is likely that the facial pattern is placed in the right hemisphere of the brain, as suggested by MRIf, CT, PET examinations (18). Pictures of a recognized face may be transferred by talented painters. We have chosen two portraits, which in our opinion perfectly document prosopgnosia (pictures 1, 2).
Picture 1: A Girl With Chrysanthemums by Olga Boznańska, 1894, Muz. Nar. Kraków. The picture is fascinating for its depth of atmosphere and for multi-meaning of the suggested contents, showing for example gentleness, anxiety and alienation (15).
Picture 2: The Portrait Of A Man by Albrecht Dürer. The essence of his mind, pride, dignity, and maturity may be seen (32).
Anosognosia may occur in the patients with both hemiplegia and hemianesthesia, and other symptoms indicating the damage of the right hemisphere. It may also occur in the patients who neglect the left side of the body (do not pay attention to the left side of the body and deny it). Anosognosia may indicate the interruption of the connection of the visual cortex to the right hemisphere or the damage of the central vestibular system (21). It is often accompanied by apraxia.
Anosognosia and unilateral neglect of the body are the examples of disruption of attention processes and indicate that the predominant lesion is in the right hemisphere. The anatomical basis of such a functional differentiation is still unclear (51).
Hemianopsia, irrespective of its causes is usually permanent, while hallucinations and illusions are often transitory. Visual hallucinations arising from the right non-dominant hemisphere occur more often than those arising in the left (dominant) hemisphere. Visual hallucinations resulting as a consequence of stroke are localized in the field of anopsia.
Illusions and hallucinations may also be caused by hyper- and hypothermia (5), cachexia, dehydration, poisoning, hypoglycaemia, hypoxia, hypnosis, serious emotional stress and religious exaltation. In children, a tendency to imagine very lively, fantasizing or ostensible "visions” may occur, falsely perceived as real phenomena (22).
Sleep disorders in children having neurological symptoms (cerebral palsy, or nocturnal, temporal, or occipital epilepsy, blindness, or breathing disorders) may coincide with somnambulism and hypnogogic hallucinations (35, 57).
In drug addicts hallucinations and illusions appear easily after taking narcotics: they may be accompanied by unusual emotional states "visions” and states similar to déjŕ vu.
Drugs that cause hallucinations are usually of herbal origin and have been used since antiquity as magic and sacred medicines, LSD (lysergic acid diethylamide) has a hallucinogenic action and is found in ergot (Claviceps purpurea). LSD causes hallucinations and illusions, time perception disorder, and psychotic disturbances.
Marihuana (an extract from the leaves and flowers of hemp (Cannabis sativa var. indica) has euphoric and hallucinogenic properties. Peyotl, found in a dried Mexican Cactus (Anhalonium levinii), contains various alkaloids, including mescalin which causes colourful hallucinations and time perception disorders, i.e. minutes seem to last for hours.
Harmine, apart from other heterocyclic alkaloids, may be found in liana (Banisteria caapi) and in Peganum harmala. It causes Parkinson-like symptoms, initiates athetotic movements and may cause colourful hallucinations.
Ibogaine – an alkaloid from the roots of Tabernanthe iboga – has euphoric and hallucinogenic properties (43, 47). Morphine (and its derivatives – heroin, codeine, and others) is the major opium alkaloid. Drug addicts use morphine in injections, or they smoke or chew it.
Euphoria after the administration of morphine is often accompanied by hallucinations and illusions. Cocaine, found in the leaves of Erythroxylon coca, causes addiction connected with hallucinations, sometimes with depression and delusions, sexual arousal and other excited states which may give in to criminal behaviour.
Atropine found in the leaves of deadly nightshade (Atropa belladonna) and in the leaves of stramonium (Datura stramonium) has stimulating properties; it may cause agitation or seizures and in poisoned patients frequently causes illusions and hallucinations.
Ecstasy and other "street drugs” have similar properties. Mescaline, LSD and amphetamines sought after by drug addicts, may be included in this. Levodope, selegiline, bromocriptine and other anti-parkinson drugs, overdosed or used with other medicines (for example with baclofen) may intensify undesirable symptoms, such as confusion, excitement, and hallucinations.
Doxepin, which inhibits adrenaline re-uptake, may infrequently cause orientation disorder and hallucinations. Amitriptyline inhibits the re-uptake of serotonin and may cause hypo-maniacal states and hallucinations. Propranolol blocks adrenergic receptors b1 and b2 and among other undesirable symptoms may cause depression, sleep disorders and hallucinations. Similarly-acting atenolol can also cause hallucinations. Albuterol (salbutamol) stimulating the b2 receptors may cause undesirable central symptoms, such as sleep disorders, excitement, and hallucinations.
Prozac inhibits serotonin and adrenaline re-uptake to neurons and may occasionally cause depressive states and hallucinations. Methysergide (Deseril, antiserotoninieum) may cause sleep disorders and hallucinations (29, 41, 48). All the above-mentioned substances can also cause hallucinations and mental disorders due to the action of true or "false” neurotransmitters.
Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.
Mam kod dostępu
- Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu albo wszystkich artykułów (w zależności od wybranej opcji), należy wprowadzić kod.
- Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.
- Aby kupić kod proszę skorzystać z jednej z poniższych opcji.
- dostęp do tego artykułu
- dostęp na 7 dni
uzyskany kod musi być wprowadzony na stronie artykułu, do którego został wykupiony
- dostęp do tego i pozostałych ponad 7000 artykułów
- dostęp na 30 dni
- najpopularniejsza opcja
- dostęp do tego i pozostałych ponad 7000 artykułów
- dostęp na 90 dni
- oszczędzasz 28 zł
1. Abraham H.D.: Visual hallucinations in macular degeneration. Am. J. Psychiatry, 1993, 150, 11:1738. 2. Aldrich M.: Cardinal Manifestations of Sleep Disorders. Chapter 38, Principles and Practice of Sleep Medicine. Edit.: Cryper M., Roth T., Dement D.C., Saunders, Philadelphia, 1989, 422. 3. Anderson R.E. et al.: Effects of glucose and PaO2 modulation on cortical intracellular acidosis, NADH redox state and infarction in the ischaemic penumbra. Stroke, 1999, 30, 1:160-70. 4. Back T.: Pathophysiology of the ischaemic penumbra – revision of the concept. Cell. Mol. Neurobiol., 1998, 8, 6:621-38. 5. Baldwin M., Hofmann A.: Hallucinations. Chapter 17. Disorders of speech, perception and symbolic behavior. Edit.: Vinken P.J., Bruyn G.W., 1980, 327-333. 6. Beale J.M., Keil F.C.: Categorical effects in the perception of faces. Cognition, 1995, 57, 3:217-239. 7. Belden J.R. et al.: Mechanisms and clinical features of posterior border-zone infarcts. Neurology, 1998, 12, 53, 6:1312-8. 8. Benson M.T., Rennie I.G.: Formed hallucination in the hemianoptic field. Postgrad. Med. J., 1989, 65:756-7. 9. Bilikiewicz T.: Psychiatria Kliniczna. PZWL, Warszawa, 1969. 10. Bing R.: Lehrbuch der Nervenkrankheiten. Benno Schwabe & Company, Basel, 1953. 11. Borruat F.X.: Visual hallucinations and illusions, symptoms frequently misdiagnosed by practitioner. Klin. Monatsbl. Augenheilkd., 1999, 214, 5:324-7. 12. Bosley T.M. et al.: Recovery of vision after ischaemic lesions: PET tomography. Ann. Neurol., 1987, 21, 5:444-50. 13. Bradley W.G. et al.: Neurology in Clinical Practice – Vol. I; Major Physiological Changes During Sleep, Approach to a common neurological problem. Butterwortg-Heinemann, Boston-Wellington, 1989. 14. Brzecki A. et al.: Illusions and hallucinations in posterior cerebral artery thrombosis – a case study. Udar mózgu. 2001, 3, 2:71-76. 15. Charazińska E., Morawińska A.: Olga Boznańska. Wydawnictwo Arkady, 1997. 16. Chen J. et al.: Visual hallucinations in a blind elderly woman: Charles Bonnet syndrome, an underrecognised clinical condition. Gen. Hosp. Psychiatry, 1996, 18, 6:453-5. 17. Cocteau J. et al.: Insania Pingens. Ciba, Basel, 1961. 18. De Renzi E. et al.: Prosopagnosia can be associated with damage confined to the right hemisphere. An MRIf and PET study and review of literature. Neuropsychology, 1994, 32, 8:893-902. 19. Fisher C.M.: Visual Hallucinations on eye closure associated with atropine toxicity. Can. J. Neurol. Sci., 1991, 18, 1:18-27. 20. Frąckowiak R.S.J. et al.: Human Brain Function: Maps of Somatosensory systems. Academic Press, 1997. 21. Geminiami G., Bottini G.: Mental representation and temporary recovery from unilateral neglect after vestibular stimulation. J. Neurol. Neurosurg. Psychiatry, 1992, 55:332-3. 22. Gregory R.: Eye and Brain. The Psychology of Seeing. Fifth Ed. Oxford Press, 1998. 23. van der Grond J. et al.: Assessment of border-zone ischaemia with a combined MR imaging-Mr-angiography-MR spectometry protocol. J. Magn. Reson. Imaging, 1999, 9, 1:1-9. 24. Hanaway J. et al.: The Brain Atlas, Fitzgerald Press Bethesda, Maryland, 1998, 202-3. 25. Jakimowicz I.: Stanisław Ignacy Witkiewicz. Auriga, 1985. 26. Kasten E. et al.: Chronic visual hallucinations and illusions following brain lesions. A single case study. Fortschr. Neurol. Psychiatr., 1998, 66, 2:49-58. 27. Kolh P. et al.: Cardiac surgery in octogenarians; peri – operative outcome and long – term results. Eur. Heart J., 2001, 22, 14:1159-61. 28. Kolmel H.W.: Complex visual hallucinations in the hemianoptic field. Neurol. Neurosurg. Psychiatr., 1985, 48, 11:20-38. 29. Kostowski W.: Podstawy Farmakologii. PZWL, 1999. 30. Lendvai D. et al.: Migraine with visual aura in developing age: visual disorders. Eur. Rev. Med. Pharmacol. Sci., 1999, 3, 2:71-4. 31. Lhermitte J.: Les hallucinations, 1951, Paris, cyt. Brain´s Diseases of the Nervous System, 8 Edit., Rev. by Walton J. M. Oxford Press, New York Toronto, 1977, 1172. 32. Lüdecke H.: Albrecht Dürer – Eine Auswahl aus seinem Werk mit einer Einleitung. Seeman Verlag, Leipzig, 1956. 33. Matthews G.G.: Neurobiologia. PZWL, Warszawa, 2000. 34. McKee A.C. et al: Peduncular hallucinosis associated with isolated infarction of the substantia nigra pars reticulata. Ann. Neurol., 1990, 27:500-4. 35. Menkes J.: Textbook of Child Neurology. Williams & Wilkins, 1998. 36. Merrit´s Neurology, 10 Edition, edit. by Rowland P., Lippincott – Wiliams & Wiliams, Philadelphia-Tokyo, 2000. 37. Meyer J.S. et al.: Sleep apnoea, narcolepsy and dreaming: regional cerebral haemodynamics. Ann. Neurol., 1980, 7, 5:479-85. 38. Mumenthaler M., Mattle H.: Neurologia. Urban & Partner, Wrocław, 2001, 408. 39. Newman R.P. et al.: Altitudinal hemianopsia caused by occipital infarctions. Clinical and computerized tomographic correlations. Arch. Neurol., 1984, 41, 4:41-8. 40. Phelps M.E. et al.: Tomographic mapping of human cerebral metabolism visual stimulation and deprivation. Neurology, 1981, 31, 5:517-29. 41. Podlewski J., Chwalibogowska-Podlewska A.: Leki Współczesnej Terapii. Split Trading, Warszawa, 1994. 42. Rauber-Kopsch F.: Lehrbuch und Atlas der Anatomie des Menschen. Band III, Nervensystem u. sienes Organe, G. Thieme, Leipzig, 1953. 43. Raymond-Hamet M.: Sur uncas remarquable d´antagonisme pharmacologique (Mediate and intermediate effects of ibogaine on the intensine), Comp. Rend. Soc. Biol., 1941, 135:176-179. 44. Riddoch G.: Dissociations of visual perception due to occipital injuries, with especial reference to appreciation of movement. Brain, 1917, 40:15-57. 45. Salamon G., Lazorthes D.G.: Atlas of the arteries of the human brain. Sandoz Editions, Paris, 1971. 46. Schiller F.: The inveterate paradox of dreaming. Arch. Neurol., 1985, 42, 9:903-6. 47. Schultes R.E., Hoffman A.: Tabernanthe Iboga. In: Schultes R.E.; Hoffman A. eds. The botany and chemistry of hallucinogenes. Sprinfield: Charles C. Thomas Publisher; 1980, 235-9. 48. Seńczuk W.: Toksykologia. Podręcznik dla studentów farmacji, PZWL, Warszawa, 1990. 49. Sichart U., Fuchs T.: Visual Hallucinationes in elderly patients with reduced vision: Charles Bonnet syndrome. Klin. Monatsbl. Augenheilk., 1992, 3:224-7. 50. Szpak G.M. et al.: Border zone neovascularisation in cerebral ischaemic infarct. Folia Neuropatholol., 1999, 37, 4:264-8. 51. Viader F.: Perception in space. Visual aspects of space perception. Rev. Neurol. (Paris), 1995, 151:8-9, 466-73. 52. Voskresenskii V.A.: Clinical signs of hypnotically suggested visual hallucinations (review). Zh. Nevropat. Psihiatr. S.S. Korsakoff., 1983, 83, 6:925-8. 53. Walton J.N.: Brain´s Diseases of the Nervous System. Revis. Oxford, Univ. Press, New York Toronto, 1977, 790. 54. Wilson B.A. et al.: Knowing where and knowing what: a double dissociation, Cortex 1997, 33, 3:529-41. 55. Zeki S.: A century of cerebral achromatopsia. Brain, 1990, 118:1721-77. 56. Zeki S.: Dynamism of a PET Image; studies of visual function. Chapter 9 w: Frackowiak R.S.J., Fried K.J., Dolan R.J., Matzziota J.C.: Human Brain Function, Academic Press, 1997, 163-82. 57. Zucconi M., Bruni O.: Sleep disorders on children with neurologic diseases. Semin. Pediatr. Neurol., 2001, 8.