A dear patient of mine who I have known for years, came in yesterday stating, “I have been seeing things.” When I asked what do you mean, she proceeded to tell me about all the things she has been seeing right after “waking up”in the morning. She is a lovely woman and very sharp, so I listened intently on her pain of seeing many unusual things every morning and also during the day.
Before I could ask, “Did you see a neurologist? Did you get an MRI? What did it & the blood test show?” She said, “First let me tell you about all I have seen. I have seen a cat and dog doing the jig and talking to each other.”
I asked her if she could hear them talking and she said, “No. I just see their mouths moving.”
She continued. “I have seen a snake across my kitchen chair. He is still there. I have seen a very vicious dog sitting on top of my bed.”
I asked when this started. She said that a few months ago, she saw a strange dog in her kitchen. She thought it was real so she called the police and had someone come get the dog. When they arrived, they thought she was crazy, but for her, the dog was still there.
She ended up seeing a neurologist who ordered an MRI which showed small vessel changes in her cortex but not clear stroke. Her carotid ultrasound and doppler showed 50% stenosis. She does have high cholesterol and is on cholesterol medications. It is likely there are possible mini-strokes that could be the cause. Her EEG did not show any seizure activity. Her blood work was normal.
She shared with me how distressing this has been and how she has cried many nights afraid to go to bed. Poor thing! She said she was petrified to sleep because she was so scared to wake up.
She continued. She said, “After you did the laser iridotomy from my narrow angles awhile ago, I started seeing little mice run across the floor on both side.” I asked if they were floaters that moved around, which are not uncommon after a laser iridotomy. She said, “No. I know what floaters are. I’ve had them for years. These were not floaters. I saw what looked like real mice running along my floor on both sides.”
This is the first case reported of experiencing a hallucination after laser iridotomy in a patient with a history of Hypnopompic Hallucinations, which might be prompted by the small laser holes we make at the 9 o’clock for the right eye and 3 o’clock position for the left eye. It has since gone away but the whole experience has been very disconcerting as the other hallucinations continue. Of note, she said, she recently went on a cruise with her daughter and they shared a room. Her daughter said that 6 of the 7 nights, this patient “talked up a storm all night long.” Thank goodness there is no tumor in her brain but there must be a way to stop these hallucinations for this patient.
In the research I did for her below. There is 1 case report of a young boy who had hallucinations and other symptoms who experienced a resolution in his symptoms by going on a Gluten Free Diet.
Thus for now, MDs will likely recommend:
1. Avoid stimulants, caffeine, etc.
2. Avoid smoking.
3. Avoid gluten
4. Avoid sugar
5. Medicines are the next tier of treatment & this is controversial given the lack of studies I could find. Your neurologist will need to review the benefits and alternatives of every option.
Sandra Lora Cremers, MD, FACS
Here is more information below.
For patients with this condition. Here are some resources that might help:
1. https://www.sleepassociation.org/patients-general-public/hallucinations-during-sleep/
2. http://neurocritic.blogspot.com/2013/12/when-waking-up-becomes-nightmare.html
The best MDs in the DC area to treat Hypnopompic Hallucinations are:
Johns Hopkins University:
Gamaldo, Charlene Edie, M.D.
Associate Professor of Anesthesiology and Critical Care Medicine
Joint Appointment in Psychiatry and Behavioral Sciences
Medical Director, Johns Hopkins Sleep Disorders Center
Boyd, Cynthia Melinda, M.D., M.P.H.
Budimirovic, Dejan B., M.D.
Attending Psychiatrist, NBU and Outpatient Child & Adolescent Psychiatry
Main co-Investigator, Clinical Trials Unit, Kennedy Krieger Institute
Medical co-Director, Fragile X Clinic
Burton, John R, M.D.
Director, Johns Hopkins Geriatric Education Center
Earley, Christopher J, M.B.B.Ch., Ph.D.
Finucane, Thomas, M.D.
Co-director, Elder House Call Program, Johns Hopkins Bayview Medical Center
Gamaldo, Charlene Edie, M.D.
Associate Professor of Anesthesiology and Critical Care Medicine
Joint Appointment in Psychiatry and Behavioral Sciences
Medical Director, Johns Hopkins Sleep Disorders Center
Harris, James C, M.D.
Joint Appointment in History of Medicine
Professor of Pediatrics
Director, Developmental Neuropsychiatry Clinic
Hughes, Abbey Jean, M.A., Ph.D.
Jun, Jonathan, M.D.
References:
| ARTICLE | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| Nature Neuroscience 1, 738 – 742 (1998) doi:10.1038/3738
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Despite recent advances in functional neuroimaging, the apparently simple question of how and where we see—the neurobiology of visual consciousness—continues to challenge neuroscientists. Without a method to differentiate neural processing specific to consciousness from unconscious afferent sensory signals, the issue has been difficult to resolve experimentally. Here we use functional magnetic resonance imaging (fMRI) to study patients with the Charles Bonnet syndrome, for whom visual perception and sensory input have become dissociated. We found that hallucinations of color, faces, textures and objects correlate with cerebral activity in ventral extrastriate visual cortex, that the content of the hallucinations reflects the functional specializations of the region and that patients who hallucinate have increased ventral extrastriate activity, which persists between hallucinations.
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Few imaging studies have investigated the conscious ‘pictures’ of the external environment that we associate with seeing (visual percepts). The problem that confronts the neuroscientist is recognizing the neural correlate of ‘seeing’ and differentiating it from afferent sensory activity, which is assumed to remain unconscious1. One solution is to study a visual system in which percepts have become dissociated from sensory input. Such dissociation can follow a sudden deterioration in visual abilities in patients who in other respects are neuropsychiatrically normal2, 3, 4. This syndrome is termed the Charles Bonnet syndrome (named after the Swiss philospher who first described it)5. The spontaneous visual percepts (visual hallucinations) experienced by these patients are identical to those associated with normal seeing, although they can be recognized because of their bizarre and often amusing character and because, given the patients’ impaired vision, they are seen in greater detail than real stimuli6. They differ from visual imagery experiences in that the hallucinations are localized to external space (rather than inside the head), have the vivid qualities of normal seeing and are not under voluntary control. We investigated the neural substrate of visual consciousness in a group of such patients, using two different but complimentary strategies, both of which have proven successful previously7, 8, 9.
The first strategy (Experiment 1) was to ask the patients to signal the onset and offset of each hallucination during a five-minute scan and to then correlate the timing of the hallucinations with the time-course of the fMRI signal. A second, indirect strategy, which did not depend on capturing a hallucination during a scan, identified functionally abnormal brain regions by scanning the patients while they viewed a nonspecific visual stimulus and comparing the results to those of a matched control group who had never experienced hallucinations (Experiment 2).
RESULTS
Visual hallucinations were reported in both experiments. Four patients had spontaneous hallucinations, whereas two others had hallucinations provoked by visual stimulation (Table 1). With the exception of one patient (PP), all hallucinations were in color. Two patients (SH, LC) reported faces, two (FP, PP) reported brickwork, fencing and map textures, and one (AK) reported objects. Unless otherwise stated, all hallucinations occurred in the central visual field. In two patients (AK and FP), Experiment 1 was repeated within the same scanning session to assess response consistency. Three patients (SH, AK, FP) with spontaneous hallucinations were unable to see the stimulus and therefore did not participate in Experiment 2. Therefore, with the exception of one patient (PP), the two experiments had different subjects.
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Spontaneous hallucinations
In all four patients with spontaneous hallucinations, the fMRI activity that correlated most significantly with the hallucination report was located in the ventral occipital lobe within or around the fusiform gyrus (Fig. 1). Colored hallucinations were associated with activity in the posterior fusiform gyrus (mean x = +28 and −35, y = −81, z = −13), whereas black-and-white hallucinations were associated with activity behind and above this region (x = 30, y = −84, z = −2). The hallucination of a face was associated with activity in the left middle fusiform gyrus (x = −42, y = −57, z = −7.5), hallucinations of objects were associated with activity in the right middle fusiform gyrus (x = 21, y = −66, z = −18), and hallucinations of textures were associated with activity around the collateral sulcus. In some experiments, additional activity was found outside ventral extrastriate cortex (for example, the frontal activation in patient FP or the activity on the medial occipital lobe in SH, shown in Fig. 1); however, this additional activity was neither consistent between repeated experiments in the same patient nor common among different patients. An increase in fMRI signal often preceded a hallucination (for example, the first, fourth and sixth hallucination shown in Fig. 2a). This temporal relationship was found in all patients studied (Fig. 2b).
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Response to visual stimulation
In Experiment 2, in patients with impaired vision who had never hallucinated, the visual stimulus evoked activity along the calcarine fissure (area V1), extending onto the ventral surface of the occipital lobe to include the fusiform gyrus (Fig. 3a). In patients with the Charles Bonnet syndrome, this stimulus evoked activity in the striate cortex but failed to do so in the fusiform and lingual gyri (Fig. 3b). We compared the corrected mean level of fMRI signal (see Methods) within the active ventral extrastriate regions in the controls with the corresponding silent regions in the patients. Mean signal was increased significantly in the hallucinators relative to the controls across the whole five-minute experiment (t = 2.94, df = 8, p < 0.025). The apparent silence of the region was due to a relatively greater increase in signal between the periods of visual stimulation (OFF) than during stimulation (ON), with a consequent degradation of periodic signal (see Methods).
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DISCUSSION
Our two sets of results converge on a single conclusion, that hallucinations of color, faces, textures and objects result from increased activity in the ventral occipital lobe. A phasic increase in activity causes a discrete hallucination (Experiment 1), whereas a tonic increase in activity decreases the response to external visual stimulation (Experiment 2). An unexpected finding was the rise in fMRI signal before the onset of the conscious experience, the opposite of the normal delayed response to visual stimulation found in fMRI experiments10, 11. Patients described the appearance and disappearance of their hallucinations as sudden (< 1 s), all-or-nothing phenomena, so the observed ‘reversed’ delay is not an artifact of uncertainty as to when to report the experience. One explanation for this finding might be that cerebral activity must exceed a certain threshold level to contribute to visual consciousness12 and that subthreshold neurophysiological activity starting 15 seconds before the hallucination is responsible for the increase in signal found at −12 seconds.
We found a striking correspondence between the hallucinatory experiences of each patient and the known functional anatomy of the occipital lobe. In patients who hallucinated in color, activity was found in the fusiform gyrus in an area corresponding to the color center, area V4 (mean x = 
28, y = −79, z = −16, see Refs 13,14), whereas in the patient who hallucinated in black and white, the activity was outside this region (posterior extent of y = −82, max z = −12, see ref 14). The descriptions of featureless colors in the hallucinations are similar to the descriptions given by patients whose ventro-medial occipital cortex has been stimulated directly15. In the patient who hallucinated an unfamiliar face, additional activity was found in the left middle fusiform gyrus, an area that responds to unfamiliar face stimuli (mean x = −35, y = −63, z = −10, see ref 16). In patients who hallucinated brickwork, fences and a map, activity was found around the collateral sulcus, an area that responds to visual textures11. Finally, in the patient who hallucinated objects, activity was found in the middle fusiform gyrus, an area that responds to visually presented objects17,18. These results are, to our knowledge, the first evidence of a correlation between the location of activity within specialized cortex and the contents of a hallucination.
Visual hallucinations are difficult to dismiss as vivid imagery experiences, as they differ both qualitatively (see Introduction) and, at least for color hallucinations, neurobiologically. (Area V4 was not differentially activated in a color imagery task compared to a spatial-orientation control task19.) The neural substrate of a color hallucination is thus closer to that of a true (non-hallucinated) percept than that of color imagery. The areas identified are unlikely to be related to the motor signaling response of the patients, as this would occur at twice the hallucination frequency (patients signaled both the onset and the offset of each hallucination), and our correlation method would thus be relatively insensitive to it. The complexity of the percepts and the absence of consistent activity in the striate cortex make it unlikely that the ventral occipital lobe is responding to spontaneous discharges in the retina or LGN. Similarly, the absence of consistent activity outside the occipital lobe argues against the hypothesis that activity in the frontal lobe is a prerequisite for conscious vision1,20 or that visual complexity in hallucinations implies activity in the anteriolateral temporal lobe15. However, our data fall short of disproving such theories. If the spatial pattern of ‘higher’ activity is not fixed for a given perceptual experience or is so diffusely distributed that its activity is not reflected in a change in fMRI signal, it would not have been detected by our method. Visual consciousness is presumably the result of complex neuronal processes with top-down influences. The results presented above suggest that such top-down complexity may be localized within each specialized area rather than being distributed across the brain.
We conclude that in patients who are neuropsychiatrically normal and in the absence of afferent sensory input, conscious percepts of color, texture, faces and objects are associated with activity in the ventral extrastriate cortex reflecting the known functional specializations of the region. Why these particular brains are functionally abnormal and whether the abnormality is common to all patients with visual hallucinations will require further investigation. These results complement previous studies of consciousness for motion12, 21and support the hypothesis that processing within each specialized visual area makes a direct contribution to conscious vision22, 23.
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METHODS
Patients and controls.
Eight patients with the Charles Bonnet syndrome (seven male, one female) were selected from a questionnaire-based study of visual hallucinations at the Institute of Psychiatry. Selection was based on (i) the frequency of stereotyped hallucinations (> 1 per day), (ii) the absence of psychiatric illness, epilepsy or cognitive impairment (MMSE > 25, ref. 24) and (iii) suitability for an MRI scan. Control patients who had never hallucinated (five males), matched for age, acuity and visual field defect, were recruited from Kings College and St Thomas’ Hospitals. All patients gave informed consent and were given psychiatric, neurological and ophthalmological assessments.
Spontaneous hallucinations.
The room lights were dimmed, and patients were asked to signal the onset and offset of each hallucination, which was recorded on a computer linked to a hand-held keypad in the scanner. One patient logged the events himself; the remaining three raised or lowered a finger while the event was logged by an investigator. Descriptions of the hallucinations were collected after each scan.
Visual stimulation.
A visual stimulus, consisting of five one-minute cycles of 30 s of visual noise (ON) followed by 30 s of a black screen (OFF), was back-projected onto a translucent screen placed over the end of the scanner bore (elongated semi-circular field, 13° vertical 
27° horizontal). The stimulus contained luminance, color, motion and form across a range of spatial and temporal frequencies. Patients were asked to attend the stimulus and to describe their hallucinations after each scan. No attempt was made to correct refractive errors.
Image Acquisition.
Gradient echo, echoplanar images (EPI) were acquired on a 1.5-Tesla GE Signa System (General Electric, Milwaukee) with an Advanced NMR operating console and quadrature birdcage headcoil for radio frequency transmission and reception. In each experiment, 100 T2*-weighted images depicting blood oxygen level-dependent (BOLD) contrast25 (TR = 3 s; TE = 40 ms) were obtained at each of 14, non-contiguous 7-mm slices (0.7 mm interslice spacing), parallel to the plane passing through the anterior and posterior commissures (AC−PC) and covering the whole brain (in-plane resolution 3 3 mm). A high-contrast, high-resolution inversion recovery EPI image (TE = 74 ms; TI = 180 ms; TR = 1600 ms; NEX = 8; voxel size = 1.5 1.5 3.3 mm) was acquired after the experiments.
Image analysis.
In Experiment 1, the time series were motion corrected26, smoothed in x and y (7-mm full width half maximum (FWHM)) and the coefficient of correlation (r) was calculated at each voxel. The process was repeated after shifting the hallucination log with respect to the fMRI time series in steps of one scan (shifts of −9 s, −6 s, −3 s, 0 s, +3 s, +6 s, +9 s) to optimize r for each patient (r max). Probability maps were calculated from the estimated rmax with 100 degrees of freedom and co-registered with the high-resolution structural image. Talairach27 coordinates were derived from transformed r max images (see below). In Experiment 2, the time series were motion corrected26, and the observed and randomized (10 permutations) fundamental power quotient (FPQ) at 0.016 Hz was estimated at each voxel28. FPQ images were transformed into Talairach space using transformation parameters derived from the structural image29. After smoothing in x and y, (20-mm FWHM), generic activation across patients was computed at each voxel by comparing the median observed FPQ with the median randomized FPQ29. Corrections for multiple comparisons were based on the number of independent voxels after smoothing. The phase of activity was calculated from sine and cosine terms in the regression model. The location of generic activation in the original, non-transformed T2*-weighted images was calculated using the transformation parameters derived above. Mean signal within the ventral occipital region of interest over (i) the whole five-minute experiment, (ii) the ON periods and (iii) the OFF periods was corrected for global intersubject differences in maximum signal across the whole slice.
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Received 22 June 1998; Accepted 24 October 1998
REFERENCES
- Crick, F. & Koch, C. Consciousness and neuroscience. Cereb. Cortex 8, 97−107 (1998). | Article | PubMed | ISI | ChemPort |
- Kölmel, H. W. Complex visual hallucinations in the hemianopic field. J. Neurol. Neurosurg. Psychiatry 48, 29−38 (1985). | PubMed | ISI |
- Lepore, F. E. Spontaneous visual phenomena with visual loss. Neurology 40, 444−447 (1990). | PubMed | ISI | ChemPort |
- Holroyd, S. et al. Visual hallucinations in patients with macular degeneration. Am. J. Psychiatry 149, 1701−1706 (1992). | PubMed | ISI | ChemPort |
- de Morsier, G. Les automatismes visuels. (Hallucinations visuelles rétrochiasmatiques). Schweiz. Med. Woch. 66, 700−703 (1936).
- Teunisse, R. J. et al. Visual hallucinations in psychologically normal people: Charles Bonnet’s syndrome. Lancet 347, 794−797 (1996). | Article | PubMed | ISI | ChemPort |
- Howard, R. J. et al. Cortical responses to exogenous visual stimulation during visual hallucinations. Lancet 345, 70 (1995). | Article | PubMed | ISI | ChemPort |
- Silbersweig, D. A. et al. A functional neuroanatomy of hallucinations in schizophrenia. Nature 378, 176−179 (1995). | Article | PubMed | ISI | ChemPort |
- Woodruff, P. W. R. et al. Auditory hallucinations and the temporal cortical response to speech in schizophrenia: A functional magnetic resonance imaging study. Am. J. Psychiatry 154, 1676−1682 (1997). | PubMed | ISI | ChemPort |
- Boynton, G. M., Engel, S. A., Glover, G. H. & Heeger, D. J. Linear systems analysis of functional magnetic resonance imaging in human V1. J. Neurosci. 16, 4207−4221 (1996). | PubMed | ISI | ChemPort |
- Puce, A. et al. Differential sensitivity of human visual cortex to faces, letterstrings, and textures: a functional magnetic resonance imaging study. J. Neurosci. 16, 5205−5215 (1996). | PubMed | ISI | ChemPort |
- Zeki, S. & ffytche, D. H. The Riddoch syndrome: insights into the neurobiology of conscious vision. Brain 121, 25−45 (1998). | Article | PubMed | ISI |
- Zeki, S. et al. A direct demonstration of functional specialization in human visual cortex. J. Neurosci. 11, 641−649 (1991). | PubMed | ChemPort |
- Mckeefry, D. J. & Zeki, S. The position and topography of the human colour centre as revealed by functional magnetic resonance imaging. Brain 120, 2229−2242 (1997). | Article | PubMed |
- Penfield, W. & Rasmussen, T. The Cerebral Cortex of Man (Macmillan, New York, 1950).
- Kanwisher, N., McDermott, J. & Chun, M. M. The fusiform face area: a module in human extrastriate cortex specialised for face perception. J. Neurosci. 17, 4302−4311 (1997). | PubMed | ISI | ChemPort |
- Sergent, J., Ohta, S. & Macdonald, B. Functional neuroanatomy of face and object processing. Brain 115, 15−36 (1992). | PubMed | ISI |
- Kanwisher, N., Chun, M. M., McDermott, J. & Ledden, P. J. Functional imaging of human visual recognition. Cog. Brain Res. 5, 55−67 (1996). | Article | ISI | ChemPort |
- Howard, R.J. et al. The functional anatomy of imagining and perceiving colour. Neuroreport 9, 1019−1023 (1998). | PubMed | ISI | ChemPort |
- Crick, F. & Koch, C. Are we aware of neural activity in primary visual cortex? Nature375, 121−123 (1995). | Article | PubMed | ISI | ChemPort |
- ffytche, D. H., Guy, C. N. & Zeki, S. Motion specific responses from a blind hemifield. Brain 119, 1971−1982 (1996). | PubMed | ISI |
- Zeki, S. A Vision of the Brain (Blackwell, Oxford, 1993).
- ffytche, D. H. & Zeki, S. Brain activity related to the perception of illusory contours. Neuroimage 3, 104−108 (1996). | Article | PubMed | ISI | ChemPort |
- Folstein, M. F., Folstein, S. E. & McHugh, P. R. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J. Psychiatry Res.12, 189−198 (1975). | Article | ChemPort |
- Kwong, K. K. et al. Dynamic magnetic resonance imaging of human brain activity during primary sensory stimulation. Proc. Natl. Acad. Sci. USA 89, 5675−5679 (1992). | PubMed | ChemPort |
- Friston, K. J. et al. Movement-related effects in fMRI time-series. Magn. Reson. Med.35, 346−355 (1996). | PubMed | ISI | ChemPort |
- Talairach, J. & Tournoux, P. Co-planar Stereotaxic Atlas of the Human Brain (Thieme, Stuttgart, 1988).
- Bullmore, E. et al. Statistical methods of estimation and inference for functional MR image analysis. Magn. Reson. Med. 35, 261−277 (1996). | PubMed | ISI | ChemPort |
- Brammer, M.J. et al. Generic brain activation mapping in functional magnetic resonance imaging: a nonparametric approach. Magn. Reson. Imaging 15, 763−770 (1997). | Article | PubMed | ISI | ChemPort |
Narcolepsy
Narcolepsy
What is narcolepsy?
What causes narcolepsy?
The cause of narcolepsy is not known. It involves the body’s central nervous system, which includes the brain and spinal cord. Narcolepsy is a genetic disorder. It is caused by a deficiency in the production of a brain chemical that helps neurons talk to each other.
What are the symptoms of narcolepsy?
-
Excessive daytime sleepiness (EDS). An overwhelming desire to sleep at inappropriate times.
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Cataplexy. A sudden loss of muscle control ranging from slight weakness to total collapse.
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Sleep paralysis. Being unable to talk or move for about one minute when falling asleep or waking up.
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Hypnagogic hallucinations. Vivid and often scary dreams and sounds reported when falling asleep.
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Automatic behavior. Performing routine tasks without conscious awareness of doing so, and often without memory of it.
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Disrupted nighttime sleep and waking up often
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Feelings of intense fatigue and continual lack of energy
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Depression
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Difficulty in concentrating and memorizing
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Vision (focusing) problems
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Eating binges
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Weak limbs
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Difficulties in handling alcohol
How is narcolepsy diagnosed?
-
Overnight polysomnogram (PSG). A sleep specialist will monitor you during an entire night of sleep.
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Multiple sleep latency test (MSLT). This test measures when you fall asleep and how quickly rapid eye movement (REM) sleep occurs.
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Genetic blood test. To test for a genetic mutation often found in people who tend to have narcolepsy.
How is narcolepsy treated?
-
Your age, overall health, and medical history
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Severity of the disease
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Your tolerance for specific medicines, procedures, or therapies
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Expectations for the course of the disease
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Your opinion or preference
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Medicines. Central nervous system stimulants are usually prescribed for excessive sleepiness. Antidepressants may help with muscle control.
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Nap therapy. Two or three short naps during the day may help control sleepiness and maintain alertness.
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Proper diet
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Regular exercise
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Behavioral therapy
Key points about narcolepsy
-
In addition to a complete medical history and physical exam, there are several lab tests to confirm the diagnosis.
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The goal of treatment of narcolepsy is to help you remain as alert as possible during the day.
-
Treatment of narcolepsy may include:
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Medicines
-
Nap therapy
-
Proper diet
-
Regular exercise
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Behavioral therapy
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Next steps
Tips to help you get the most from a visit to your healthcare provider:
-
Know the reason for your visit and what you want to happen.
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Before your visit, write down questions you want answered.
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Bring someone with you to help you ask questions and remember what your provider tells you.
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At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
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Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
-
Ask if your condition can be treated in other ways.
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Know why a test or procedure is recommended and what the results could mean.
-
Know what to expect if you do not take the medicine or have the test or procedure.
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If you have a follow-up appointment, write down the date, time, and purpose for that visit.
-
Know how you can contact your provider if you have questions.
J Neuroophthalmol. 2010 Sep;30(3):272-5. doi: 10.1097/WNO.0b013e3181e05340.
Hallucinations: A Systematic Review of Points of Similarity and Difference Across Diagnostic Classes
- ↵*To whom correspondence should be addressed; School of Psychiatry and Clinical Neurosciences, The University of Western Australia, 35 Stirling Highway Perth, Western Australia 6009, Australia; tel: +61-8-9341-3685, fax: +61-9384-5128, e-mail: flavie.waters@health.wa.gov.au
Abstract
A functional magnetic resonance imaging investigation of visual hallucinations in the human striate cortex.
Author information
- 1Quaid-e-Azam University, Islamabad, Pakistan.
- 2University of Gujrat, Gujrat, Pakistan. dr.fayyaz@uog.edu.pk.
- 3Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
- 4University of Gujrat, Gujrat, Pakistan.
- 5Lahore University of Managment Sciences, Lahore, Pakistan. safeeullah@lums.edu.pk.
Abstract
PURPOSE:
METHODS:
RESULTS:
CONCLUSIONS:
Matter is nonmaterial. arises from, but is independent of the brain. This gives
humans free will.
same substance. Thought stops existing
when the body dies
Effect
stimuli, even if we don’t consciously remember seeing it
questions they’ve seen before, even if they don’t remember it
information. Behavior demonstrates that at another level there is awareness.
environment
of Consciousness
of the present moment. You are aware of something on the outside as well as
some specific mental functions happening on the inside. For example, you are aware
of your environment, your breathing, or the chair that you are sitting on.
us off from the other species on the planet.
It is an awareness of ourselves, but it is also an awareness of our own
mortality. We realize that this state of
being can stop at any time. Since we are
aware of our own impermanence, we have constructed many theories and ideas that
focus on the continuation of our consciousness.
This can be either a belief in ghosts or religion but all aid us in a
search for immortality.
the preconscious mind consists of accessible information. You can become aware
of this information once your direct your attention to it.
to your house without consciously needing to be alert to your surroundings. You
can talk on the cell phone and still arrive home safely. You can easily bring
to consciousness the subconscious information about the path to your home. You
can also easily remember phone numbers that you frequently use.
unconscious becomes subconscious, and then conscious (e.g. a long-forgotten
childhood memory suddenly emerges after decades). We can assume that some
unconscious memories need a strong, specific trigger to bring them to
consciousness; whereas, a subconscious memory can be brought to consciousness
more easily.
primitive, instinctual wishes as well as information that we cannot access.
Although our behaviors might indicate the unconscious forces that drive them,
we don’t have easy access to the information stored in the unconscious mind.
During our childhood, we acquired countless memories and experiences that
formed who we are today. However, we cannot recall most of those memories. They
are unconscious forces (beliefs, patterns, subjective maps of reality) that
drive our behaviors.
mind has always raised interesting questions. Why are they hidden? From an evolutionary perspective, the Unconscious
is understandable. It is a well of
ancient primeval drives that once kept us alive but now are socially
unacceptable. But the Subconscious is
more problematic. Why isn’t this
information readily apparent? Why hide
it?
rhythm
different levels of sleepiness and alertness throughout the day, but what
causes these patterns?
homeostasis and the circadian biological clock .
sleep/wake homeostasis tells us that a need for sleep is accumulating and that
it is time to sleep. It also helps us maintain enough sleep throughout the
night to make up for the hours of being awake. Sleep/wake homeostasis
creates a drive that balances sleep and wakefulness.
on the other hand, regulate the timing of periods of sleepiness and wakefulness
throughout the day.
the day, so adults’ strongest sleep drive generally occurs between 2:00-4:00 am
and in the afternoon between 1:00-3:00 pm. The circadian rhythm also causes us
to feel more alert at certain points of the day.
when most teens experience a sleep phase delay. This shift in
teens’ circadian rhythm causes them to naturally feel alert later at night,
making it difficult for them to fall asleep before 11:00 pm.
other commitments, this sleep phase delay can make it
difficult to get the sleep teens need — an average of 9 1/4 hours, but at
least 8 hours. This sleep deprivation can influence the circadian rhythm.
strongest circadian “dips” tend to occur between 3:00-7:00 am and 2:00-5:00 pm,
but the morning dip (3:00-7:00 am) can be even longer if teens haven’t had
enough sleep, and can even last until 9:00 or 10:00 am.
the brain called the Suprachiasmatic Nucleus (SCN), a
group of cells in the hypothalamus that respond to light
and dark signals. From the optic nerve of the eye, light travels to the SCN,
signaling the internal clock that it is time to be awake. The SCN signals to
other parts of the brain that control hormones, body temperature and other functions
that play a role in making us feel sleepy or awake.
signals to raise body temperature and produce hormones
like cortisol.
The SCN also responds to light by delaying the release of other
hormones like melatonin, which is associated with sleep onset and is produced
when the eyes signal to the SCN that it is dark.
with our natural sleep patterns, since the shift in time and light cues on the brain
forces the body to alter its normal pattern to adjust.
into sleep. Sleep onset usually transmits into non-rapid eye movement sleep
(NREM sleep) but under certain circumstances (e.g. narcolepsy, infancy) it is
possible to transmit from wakefulness directly into rapid eye movement sleep
(REM sleep).
Imagery – images and
experiences during the moments following the transition from wake to sleep
for a short period of time, usually occurs out of REM (dream) sleep
The brain produces Theta
waves and they get slower and higher in amplitude as we approach Stage 2. Sleep spindles are brief bursts of fast
brainwave activity occur in this period.
sleeping. Typically, more time is spent in stage 2 sleep than in light sleep,
deep sleep or dream sleep. Sleep spindles are brief bursts of fast brainwave activity occur in this
period. The greatest spindle activity occurs at
the beginning and the end of the non-REM portion of the sleep cycle
waves, the deeper the sleep. Delta waves
are produced in these periods. This is the time of REM sleep.
minutes throughout the night, and it accounts for up to 20-25% of total sleep
time, although the proportion decreases with age (a newborn baby may spend 80%
of total sleep time in the REM stage).
suggests, it is associated with rapid (and apparently random) side-to-side
movements of the closed eyes. This eye motion is not constant but intermittent.
known exactly what purpose this movement serves, but it is believed that the
eye movements may relate to the internal visual images of the dreams
that occur during REM sleep, especially as they are associated with brain wave
spikes in the regions of the brain involved with vision.
during REM sleep is largely characterized by low-amplitude
mixed-frequency brain waves, quite similar to those experienced during the
waking state – theta waves, alpha waves and even the high frequency beta waves
more typical of high-level active concentration and thinking. Because of the
similarities with the waking state, REM sleep has earned the moniker “paradoxical
sleep”.
oxygen consumption, reflecting its energy consumption, is also very high during
this period, in fact often higher than when awake and working on a complex
problem. Breathing becomes more rapid and irregular during REM sleep
than during non-REM sleep, and the heart rate and blood pressure also increase
to near waking levels. Core temperature is not well regulated
during this time and tends towards the ambient temperature, in much the same
way as reptiles and other cold-blooded animals. Sexual arousal is also
common during REM sleep regardless of whether or not any dreams in progress are
of an erotic nature.
become more relaxed during non-REM sleep, they become completely paralyzed and
unresponsive during REM sleep. This virtual absence of muscle tone and
skeletal muscle activity is known as atonia, and it occurs because the
brain impulses that control muscle movement are completely suppressed (other
than those controlling the eye movements and one or two other essential
functions, like the heart, diaphragm, etc, that allow us to breathe and remain
alive).
dreams – certainly the most memorable and vivid dreams – occur during REM
sleep, and it is thought that the muscular atonia that accompanies it may
be a built-in measure to protect us from self-damage which could occur while
physically acting out these vivid REM dreams. This hypothesis is borne
out by Michel Jouvet’s early experiments on cats in which the muscle
inhibition nerves were severed, leading these cats to physically stalk
invisible prey and run and jump around wildly during the dreams of REM sleep.
sleep, we will spend more time in REM the following night.
disorder – technically known as a somnipathy or dyssomnia – is any
medical disorder which negatively affects a person’s healthy sleep patterns.
Usually this involves less than adequate sleep to the extent that this may
interfere with the person’s normal physical, mental and emotional functioning,
but excessive
sleep (such as in hypersomnia and narcolepsy) can also be a problem. At
least seventy, or by some counts over a hundred, different disorders that can
affect sleep have been identified, the most common and well-known being insomnia,
sleep apnea and restless legs syndrome.
very common complaint – indeed, the most commonly diagnosed sleep disorder –
affecting some 30% to 50% of the general population according to some
estimates, with about 10% of the population suffering from long-standing or
chronic insomnia. It can occur at any age, but is most common in the elderly.
It is also generally more common among women than men.
cause of episodic or transient insomnia is stress and anxiety, whether
from school- or job-related pressures, family or marriage problems, serious
illness or death in the family, etc.
insomnia is not managed properly, it can morph into a long-term problem,
persisting long after the original stress has passed. Most insomniacs tend to
be anxiety-prone by nature. At the extreme end of the scale, there
is a very rare genetic sleep disorder called fatal familial insomnia (FFI),
which appears in a handful of families in late adulthood, and which is in fact
quite as fatal as the name suggests. In FFI, malformed proteins called prions
attack the thalamus, an organ in the brain that plays a major role in
regulating sleep. The sufferer gradually completely loses the ability to sleep,
first the ability to nap and then the ability to sleep at night. Hallucinations
soon follow, then rapid weight loss and dementia, and finally complete
unresponsiveness. Within a year of striking, the disease causes death
neurological disorder that affects the control of sleep and wakefulness. People
with narcolepsy experience excessive daytime sleepiness and intermittent,
uncontrollable episodes of falling asleep during the daytime. These
sudden sleep attacks may occur during any type of activity at any time of the
day.
suffering from narcolepsy, REM sleep occurs almost immediately in the sleep
cycle, as well as periodically during the waking hours. Narcolepsy usually
begins between the ages of 15 and 25, but it can become apparent at any age.
What Causes Narcolepsy?
narcolepsy is not known; however, scientists have made progress toward
identifying genes strongly associated with the disorder. Some experts think
narcolepsy may be due to a deficiency in the production of a chemical called
hypocretin by the brain What Are the Symptoms of Narcolepsy?
daytime sleepiness (EDS)
interferes with normal activities on a daily basis, whether or not a person
with narcolepsy has sufficient sleep at night. People with EDS report mental
cloudiness, a lack of energy and concentration, memory lapses, a depressed
mood, and/or extreme exhaustion.
muscle tone that leads to feelings of weakness and a loss of voluntary muscle
control. It can cause symptoms ranging from slurred speech to total body
collapse, depending on the muscles involved, and is often triggered by intense
emotions such as surprise, laughter, or anger.
vivid and frequently frightening. The content is primarily visual, but any of
the other senses can be involved. These are called hypnagogic hallucinations when
accompanying sleep onset and hypnopompic hallucinations when they occur during
awakening.
insomnia – causes you to stop breathing for short periods of time at night -wake
up slightly and gasp for air – won’t remember waking – affects attention, memory, energy – prevents
deep sleep – high risk group: overweight men (Fisher)
and somnambulism (sleep walking)
children – early in the night; stage 4 – not remembered in the morning
We May Dream Because of Random Impulses
& McCarley put forward some dream research that said that dreaming is the
result of random impulses coming from the brain stem.
machine, the researchers were able to track the regular REM states of people
during sleep. They used this data to form a predictable mathematical model and
conclude that dreaming is a freak physiological (bodily) occurrence – rather
than a psychological function.
them, the fact that we see images and hear sounds in our dreams is simply the
brain’s way of understanding noisy electrical signals. They said that dreams
are random and meaningless.
We May Dream to Organize The Brain
de-clutter our brains. Every day we are bombarded with new information, both
consciously (eg learning) and unconsciously (eg advertising).
dream theory suggests dreaming is a way to file away key information and
discard meaningless data. It helps keep our brains organized and optimizes our
learning. This theory hasn’t been proven by dream research. If it were 100%
correct, our entire day would be replayed to us during our REM sleep!
theory also point out that our brains are not the same as computers, and to
draw a comparison to filing, processing and storage space is likely to be
inaccurate. They also point out that although some of our dreams relate back to
the waking day (Freud called this “day residue”), the majority of our
dreams are not about real world events.
We May Dream to Help Solve Problems
researchers think that dreams are for mental and emotional problem solving.
that our dreams help us to register very subtle hints that go unnoticed during
the day. This explains why “sleeping on it” can provide a solution to
a problem.
there are also arguments against this theory of dreaming. For a start, most
people only remember a very small number of their dreams.
We May Dream to Cope With Trauma
way of coping with trauma. Based on the intensity of our emotions, we will
generate dreams to cope with certain situations.
if you escape from a house fire and the experience shakes you up, chances are
you will dream about it that night. The more traumatic the event, the more
emotions are felt, and the more important it is to get over it. Dreaming about
the fire will help you come to terms with what happened and prepare you for it
ever happening again.
doesn’t explain why we dream of fantastic or mundane things – only that
nightmares can be a kind of rehearsal for trauma.
psychoanalysis
analysis emphasizes dream interpretation as a way to uncover information in the
unconscious mind. Dreams are seen as
wish fulfillment. In dreams we act out
our unconscious desires
on two main factors:
dream. This is to make the patient aware
of their own role in constructing the dream.
the symbols in the dream.
trusted because the ego protects us from information in the unconscious
mind. He called it “protected sleep”
theory
Hobson emphasizes the role of neurochemicals in the brain and random electrical
impulses originating in the brainstem. He
once stated that dreams are the random firing of neurons, he has since updated
this view to say that dreams are the brain’s cobbled attempt at making sense of
them.
Freud had it wrong. He may even have impeded our scientific understanding of
the nature of dreams by propagating such ominous theories. Hobson is all for a
psychological meaning to dreams, but just that it needn’t be locked away under
layers of secretive unconscious meaning. Instead, Hobson takes a Jungian
approach: dreams reveal far more than they hide – and can actually be highly transparent.
However, it’s difficult to link this conclusion to Hobson’s biological
explanation for dreaming.
does make sense. Next time you dream of being chased, isn’t it likely that you
are – metaphorically – running away from something in real life that’s causing
you anxiety? And if you dream of being pregnant – for a woman at least – is
this a natural expression of your desire to have babies?
brain’s interpretation of what is happening physiologically during REM sleep
function of REM is to integrate information processed during the day into our
memory
the number and the intensity of our dreams, dream content often relates to
daily concerns, babies REM more
of Dreams
theories have been suggested to account for the occurrence and meaning of
dreams. The following are just of few of the proposed ideas:
Stimuli theory suggests that dreams are the result of our brains trying
to interpret external stimuli during sleep. For example, the sound of the radio
may be incorporated into the content of a dream
theory uses a computer metaphor to account for dreams. According to this
theory, dreams serve to ‘clean up’ clutter from the mind, much like clean-up
operations in a computer, refreshing the mind to prepare for the next day.
model proposes that dreams function as a form of psychotherapy. In this theory,
the dreamer is able to make connections between different thoughts and emotions
in a safe environment
Amnesia is literally the process of forgetting events that occurred while you
were under hypnosis
is a suggestion that a hypnotized person behave in a certain way after hypnosis
ends
hypnosis work?
person because they are expected to
Are prone to involuntary movement
Have rich fantasy lives
Can focus intensely on a single task for a long time
which allows for loss of time.
Are able to suspend their critical judgment and accept
incongruous answers to problems.
Follow directions well to the point of compulsive
compliance
Theory
suggestions of the hypnotist on another level they retain an awareness of
reality
presence of a hidden observer. This
could be a level of our consciousness that monitors what is happening while
another level obeys the hypnotist
paranormal and psychic phenomena which includes telepathy, precognition,
clairvoyance, psychokinesis, near-death experiences, reincarnation,
apparitional experiences, and other paranormal claims
institutions in several different countries and funded through private
donations, and the subject rarely appears in mainstream science journals.
programs.
of Edinburgh
Hope University
Psychological Processes at the University of Northampton
Research Unit at Goldsmiths University of London.
University
of Arizona
but not limited to:
information on thoughts or feelings between individuals by means other than the
five classical senses.
information about future places or events before they occur.
information about places or events at remote locations, by means unknown to
current science.
of the mind to influence matter, time, space, or energy by means unknown to
current science.
experiences: An experience reported by a person who nearly died, or
who experienced clinical death and then revived.
experiences: Phenomena often attributed to ghosts and encountered in
places a deceased individual is thought to have frequented, or in association
with the person’s former belongings.
natural explanations resulting from psychological and physical factors
parapsychology is in terms of the aims of what each discipline is about.
evidence to prove the reality of paranormal forces, to prove they really do
exist. So the starting assumption is that paranormal things do happen.
that paranormal forces probably don’t exist and that therefore we should be
looking for other kinds of explanations, in particular the psychological
explanations for those experiences that people typically label as paranormal.
anomalistic psychology has been reported to be on the rise. It is now offered
as an option on many psychology degree programs
Drugs
an altered state of consciousness. Examples include tobacco, alcohol, cannabis,
amphetamines, ecstasy, cocaine, and heroin.
according to their pharmacological effects. Commonly used psychoactive drugs
and groups:
that wake one up, stimulate the mind, and may even cause euphoria, but do not
affect perception – Examples: amphetamine, caffeine, cocaine, nicotine
and narcotics. This category includes all of the calmative, sleep-inducing,
anxiety-reducing, anesthetizing substances, which sometimes induce perceptual
changes, such as dream images, and also often evoke feelings of euphoria.
barbiturates, benzodiazepines.
deliriants. This category encompasses all those substances that produce distinct
alterations in perception, sensation of space and time, and emotional states
nitrous oxide.
person’s neurochemistry, which in turn causes changes in a person’s mood,
cognition, perception and behavior.
neurotransmitter systems are called agonists. They act by increasing the
synthesis of one or more neurotransmitters, by reducing its reuptake from the
synapses, or by mimicking the action by binding directly to the postsynaptic
receptor.
antagonists, and operate by interfering with synthesis or blocking postsynaptic
receptors so that neurotransmitters cannot bind to them.
the structure and functioning of neurons, as the nervous system tries to
re-establish the homeostasis disrupted by the presence of the drug
can increase the number of receptors for that neurotransmitter or the receptors
themselves may become more responsive to neurotransmitters; this is called
sensitization.
neurotransmitter may cause a decrease in both number and sensitivity of these
receptors, a process called desensitization or tolerance.
dependence and addiction. Physical dependence on antidepressants or anxiolytics
may result in worse depression or anxiety, respectively, as withdrawal
symptoms. Unfortunately, because clinical depression (also called major
depressive disorder) is often referred to simply as depression, antidepressants
are often requested by and prescribed for patients who are depressed, but not
clinically depressed.
Reversible blindness: simple partial seizures presenting as ictal and postictal hemianopsia.
Author information
- 1Department of Neurology, Georgetown University Hospital, Washington, District of Columbia 20007, USA. pt.ghosh@yahoo.com
Abstract
Improvement in Psychotic Symptoms After a Gluten-Free Diet in a Boy With Complex Autoimmune Illness
DISCUSSION
Acknowledgments
REFERENCES
Visual hallucination and tremor induced by sertraline and oxycodone in a bone marrow transplant patient.
Author information
- 1Department of Pharmacology and Medicine, Division of Clinical Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA.
Abstract
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| Nature Neuroscience 1, 738 – 742 (1998) doi:10.1038/3738 The anatomy of conscious vision: an fMRI study of visual hallucinations
Despite recent advances in functional neuroimaging, the apparently simple question of how and where we see—the neurobiology of visual consciousness—continues to challenge neuroscientists. Without a method to differentiate neural processing specific to consciousness from unconscious afferent sensory signals, the issue has been difficult to resolve experimentally. Here we use functional magnetic resonance imaging (fMRI) to study patients with the Charles Bonnet syndrome, for whom visual perception and sensory input have become dissociated. We found that hallucinations of color, faces, textures and objects correlate with cerebral activity in ventral extrastriate visual cortex, that the content of the hallucinations reflects the functional specializations of the region and that patients who hallucinate have increased ventral extrastriate activity, which persists between hallucinations.
Few imaging studies have investigated the conscious ‘pictures’ of the external environment that we associate with seeing (visual percepts). The problem that confronts the neuroscientist is recognizing the neural correlate of ‘seeing’ and differentiating it from afferent sensory activity, which is assumed to remain unconscious1. One solution is to study a visual system in which percepts have become dissociated from sensory input. Such dissociation can follow a sudden deterioration in visual abilities in patients who in other respects are neuropsychiatrically normal2, 3, 4. This syndrome is termed the Charles Bonnet syndrome (named after the Swiss philospher who first described it)5. The spontaneous visual percepts (visual hallucinations) experienced by these patients are identical to those associated with normal seeing, although they can be recognized because of their bizarre and often amusing character and because, given the patients’ impaired vision, they are seen in greater detail than real stimuli6. They differ from visual imagery experiences in that the hallucinations are localized to external space (rather than inside the head), have the vivid qualities of normal seeing and are not under voluntary control. We investigated the neural substrate of visual consciousness in a group of such patients, using two different but complimentary strategies, both of which have proven successful previously7, 8, 9.
Spontaneous hallucinations
Response to visual stimulation
DISCUSSION
METHODS
Received 22 June 1998; Accepted 24 October 1998
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