Visual hypo and hypergnosia as exemplars of poles of

Behavioural Neurology 19 (2008) 153–168 153IOS Press

Visual hypo and hypergnosia as exemplars ofpoles of psychic tonus in the occipital lobes:Multiple case analyses

Claude M.J. Braun∗ and Anik GuimondInstitut de Sciences Cognitives and Department of Psychology, Universit e du Quebec a Montreal, Montreal,Canada

Abstract. The “psychic tonus” model or PTM [1] of hemispheric specialization states that the left hemisphere is a psychic andbehavioral activator and that the right hemisphere is an inhibitor. The PTM predicts that the tonus of visual representation oughtto manifest hemispheric specialization in the occipital lobes. Specifically PTM predicts that pathological positive visual tonus(visual hallucination) ought to be associated more frequently with right occipital lesions. PTM also predicts that pathologicalnegative visual tonus (loss of visual imagery) ought to result more often from left occipital lesions. We reviewed 78 cases ofpost lesion hallucination and 12 cases of post lesion loss of evocation of images, all following a unilateral lesion. Analyses ofthese relevant previously published cases support the predictions. In accordance with previously published demonstrations ofhemispheric specialization for auditory tonus in the temporal lobes and for somesthetic tonus in the parietal lobes, the presentfindings extend the psychic tonus model of hemispheric specialization to vision in the occipital lobes.

Keywords: Visual representation, hallucination, psychic tonus, hemispheric specialization, hypognosia

1. Introduction

1.1. Psychic tonus: A hemispheric specializationinterpretation of positive and negative symptoms

Braun [1] has developed a model of hemispheric spe-cialization principally based on effects of focal lesionswhich he has termed “psychic tonus”. This model pro-poses a new framework for interpretation of positiveand negative behavioral symptoms. The model drawsequally from psychiatry as it does from neurology aswell as biopsychology of normal function in humansand animals. The model is based on demonstrations tothe effect that psychomotor baseline [2,3], libido [3,4],

∗Corresponding author: Claude M.J. Braun, PhD, Professeur titu-laire, Centre de Neurosciences Cognitives, UQAM, C.P 8888, Succ.Centre-Ville, Montreal, Quebec, Canada, H3C 3P8. Tel.: +514987 3000 (4814); Fax: +514 987 8952; E-mail: [email protected]; URL: http://www.er.uqam.ca/nobel/r31210/home.html.

talkativeness [3,5], immune function [6], memory [7],audition [8] and somesthesia [9] are all modulated insimilar opposed ways by the two hemispheres in righthanders. The normal left hemisphere increases psychictonus while the right decreases it.

The model predicts that post lesion visual anoma-lies should also manifest the same (opposite) dissocia-tion according to lesion side. Left hemisphere lesionsshould produce negative visual anomalies (dulling ofvisual representation, i.e., of imagination) because ofdirect loss of the specialized circuitry of the damagedhemisphere. Right hemisphere lesions should producepositive visual anomalies such as hallucinations due torelease of the specialized circuitry of the undamagedhemisphere. It is unusual but not unheard of [10] fordulling or loss of perceptual representations and hallu-cinations to be considered flip sides of a same coin. Tomake this point clear we will term positive distortion ofperception “hypergnosia” and negative distortion “hy-pognosia”. A mental image can be disturbed in twodirections on a continuum. It can be over-excitable too

ISSN 0953-4180/08/$17.00 2008 – IOS Press and the authors. All rights reserved

154 C.M.J. Braun and A. Guimond / Visual perceptual tonus and the cerebral hemispheres

lush, too rich, too driven, hypertonic, i.e., hypergnosicon the one hand. However it can be under-excitable,frugal, impoverished, sluggish, hypotonic, i.e., hyp-ognosic on the other. The former, in extreme form,is none other than visual hallucination. The latter, inextreme form, is none other than the loss of visual im-agery (in the presence of intact reception sensation andelementary visual perception).

1.2. Disorders of visual perception

Short term visual memory and imagination are bare-ly distinguishable constructs. There have been manyfunctional imaging investigations of encoding of visualmaterial, verbal or non verbal. Regarding lateraliza-tion of the activations reported, there is a strong con-stant. The left hemisphere is practically always activat-ed more than the right during encoding into memory(see Cabeza & Nyberg [11], for a meta-review). Per-haps not surprisingly, this has been many times reportedfor verbal material. More surprisingly, the same hemi-spheric asymmetry has consistently been reported fornon verbal material as well [11]. Some of this asymme-try has been interpreted as an effect of semantic (verbal)processing which is thought to occur even when partic-ipants are encoding non verbal material [11]. Farah andcolleagues [12] reviewed a series of case reports of lossof “visual imagery” (in both visual fields) and conclud-ed that the trend was indicative of a higher frequencyof left hemisphere lesions. Goldenberg and Artner [13]tested visual imagery and other functions in groups ofpatients with right and left posterior cerebral artery le-sions. They concluded that left hemisphere lesionedpatients indeed had poorer visual imagery than righthemisphere lesioned patients but that this was due to aloss of visual knowledge about the objects rather thana loss of imagery per se. The same explanation comesup in reviews of findings to the effect that left hemi-sphere lesions cause memory impairment, including ofnon verbal material, far more often than right hemi-sphere lesions (see Gillespie, Bowen and Foster [14] fora meta-analysis of the literature). However, that argu-ment does not explain why the left hemisphere is foundto contribute more to memory than the right in animals(see Braun [1], for a review of that literature). To sumup, functional imaging and the anatomoclinical methodboth support a strong left hemispheric specialization forvisual imagination or encoding into memory. Researchwith animals demonstrates that this hemispheric asym-metry is not entirely due to verbal-semantic processingduring encoding or during imagination.

Visual hallucination is rarer than auditory orsomesthetic hallucination, and thus functional imagingstudies of visual hallucination are less numerous thanof hallucination in those other modalities. Only onestudy [15] has investigated visual hallucination in largegroups of patients with good sets of hallucinatory inci-dents. Oishi and colleagues [15] compared two groupsof patients with Parkinson’s disease (PD), a subgroupwith visual hallucinations (N = 24) and another with-out (N = 41) using rCBF. They found right fusiformhypometabolism in the hallucinating group. Nagano-Saito and colleagues [16] also compared a few PD pa-tients with and without visual hallucinations. Theyfound left frontal activation in the hallucinating cases.O’Brian and colleagues [17] studied hallucination ina few patients with Lewy body dementia (LBD) us-ing SPECT. They reported a correlation between leftcingulate and parietal hypometabolism and visual hal-lucinations. Imamura and colleagues [18] carried outa similar study and reported right parietal and tempo-ral activation in the hallucinating cases, not significantwhen controlled for multiple comparisons. Mori andcolleagues [19] reported a similar study as well, andfound no evidence of lateralization of activations. Inthese latter three studies of LBD there seemed to be veryfew hallucinating cases, and very few hallucinatory in-cidents, suggesting to us that these results should not bejudged informative for hemispheric specializations inthe normal brain. Adachi and colleagues [20] studiedvisual hallucination in five patients with Charles Bon-net syndrome (cases without focal brain lesions). Im-portantly, SPECT measurements were obtained whenpatients were and were not hallucinating. Hallucina-tions were clearly related to activations, particularlyin the temporal lobes, but these activations occurredequally often in either hemisphere. Shedlack and col-leagues [21] found MRI stigmata in 12 elderly CharlesBonnet patients, but there was no evidence of any asym-metry of the stigmata. Braun and colleagues [22] re-viewed single case reports of post lesion visual hallu-cination and found that of 55 cases due to a unilater-al brain lesion 35 presented a right hemisphere lesion(p < 0.05). In that review the intrahemispheric locationof the lesion was unconstrained and the field in whichhallucinations were experienced was not noted. To sumup, the functional imaging and lesion literatures on vi-sual hallucination are not yet very informative aboutoccipital lateralization, but the most credible evidenceavailable [15,22] suggests a source weakly lateralizedto the left hemisphere.

C.M.J. Braun and A. Guimond / Visual perceptual tonus and the cerebral hemispheres 155

1.3. Statement of purpose

This project proposes to optimize exploitation ofmultiple case analysis to test the idea according towhich hemispherically specialized psychic tonus wouldbe a good explanation of hypergnosia and hypognosiain the visual modality expressed exclusively in the oc-cipital lobes. To this end carefully selected unilateralpost-lesion cases were reviewed using a classificationsystem appropriate for the inference test foreseen atoutset.

2. Method

Cases sought here were 1) non paroxystic cases ofvisual hallucination (in one or both fields) due to a uni-lateral lesion involving the occipital lobe 2) non parox-ystic cases of selective loss of visual imagery in bothfields in the awake subject due to a unilateral lesioninvolving the occipital lobe. All cases manifesting anyepileptic sign (seizures or twitching or drop attacks orEEG paroxysm or evidence of successful control ofthe hallucinations with anticonvulsants) were exclud-ed from this study because hallucinations can comefrom an ipsilesional paroxysm even in presence of amassive lesion (see [23] for an excellent demonstrationof the latter). Manifestation of the target symptom ofboth groups was an exclusion criterion. EEG findings,presence of aphasia, the field in which the hallucina-tion occurred, the simple (unformed) versus complex(formed) nature of the hallucination, evidence of obvi-ous episodic memory content in the hallucintation, pa-tient age, gender and hand preference, lesion locationand etiology of the lesion, were all noted systematicallyfor each case, in view of control analyses.

Each of these data bases will be submitted to a sameconservative non parametric inference test (two tailedChi2 test) of preponderance of right or left sided le-sions. Right hemisphere lesions are expected to pro-duce hypergnosia (hallucinations) and left hemispherelesions are expected to produce hypognosia (loss ofimagination). As a side issue, we were interested in in-directly testing the idea according to which perilesional(i.e., ipsilesional) hypermetabolism could explain uni-lateral hallucinations. Perilesional hypermetabolismhas been reported in several cases of unilateral hallu-cination [24–26], including selectively during halluci-nation [27–29]. In such cases, hallucinations are oc-casionally suspected of being irritative and paroxysticin nature [27]. However, ipsilesional hypometabolism

has been more frequently reported [30–35], includingselectively during the hallucinations [36,37]. In suchcases, hallucinations are not (or are less) suspectedof resulting from paroxystic activity. Contralesionalhypermetabolism has been reported in a case with visu-al hallucinations [38], but this seems to be an unusualfinding. We reasoned that if the perilesional releaseaccount of post lesion hallucination in a single fieldis the best explanation, then the majority of cases ofunilateral hallucination should manifest their halluci-nations in the contralesional (usually partially anopic)field, as noted initially by Kolmel in his review of 16patients [39]. Given as much, we were interested in de-termining whether a psychic tonus effect (i,e., a lesionside effect), in the cases with hallucination, would belimited to cases with bilateral hallucinations, with com-plex hallucinations or with hallucinations laden withcontent from episodic memory, all more apt to reflecthigher order hemispheric specialization. Though wesuppose that a hemispheric specialization effect oughtto be due to contralesional release, we planned to testthat notion, if possible, with EEG findings (i.e., ipsile-sional slowing) and cases with SPECT imaging.

3. Results

3.1. Positive disorders of visual perception

Cases with post-lesion visual hallucination weresought by means of multitudes of medline and googlescholar searches and cross referencing from relatedreadings. For purposes of testing the psychic tonusmodel, cases with hallucinations in both visual fieldsare in principle more interesting than cases with hallu-cinations in a single field. Indeed to the extent that sucha specific experience as hallucination can be conceivedas a peculiar manifestation of unbridled mentation, i.e.,elevated mental tonus, then the hallucination is all themore plausibly interpreted as such if it invades bothvisual fields – precluding its interpretation as a banalcontralesional effect. Along the same line of reasoning,cases with complex hallucinations and/or hallucinatedelements drawn from episodic memory (a hallucina-tion of one’s mother for example) are more relevant inprinciple for testing the psychic tonus model becausethese phenomena more readily reflect a “general” men-tal state than a small unformed hallucination (e.g., aspot of light) occurring in the anoptic field. Also, caseswith comfirmed slowing of EEG over the lesion and bythe same stroke rejection of the hypothesis of an irrita-


Table 1Non-paroxystic visual hallucinations in both visual fields following a radiologically or surgically objectified unilateral occipital lobe lesion

Age at onsetgender andhand preference

Locus ofthe lesion

Lesionetiology

Type of hallucination and locationin the visual field(s)* = the hallucinated image is fromepisodic memory

Clinical considerations Reference

71 FemaleH?

Rightoccipital

Infarct Complex visual hallucinations*in both visual fields

No EEG, seizures or psychiatriccomorbidity reported

[61]Michel& Troost

73FemaleH?

Rightoccipito-temporal



[62]Meadows& Munro

66 FemaleH?

Rightoccipital

Infarct Complex visual hallucinationsin both visual fields

No EEG or seizures reported,reactive depression, psychosis,paranoia and delusions

[63]Mancusa& Cole

70 FemaleH?

Leftoccipital



[64]Lance

75 MaleH?

Leftoccipital



[39]Kolmel

72 FemaleRH

Rightoccipital

Infarct Complex visual hallucinations,apparently in both visual fields

Four EEGs revealed no paroxysmalactivity, only slowing over the lesion,no seizures were observed, pre-strokepsychiatric status was normal

[65]Peroutkaet al.

77 MaleRH

Rightoccipital



[66]Doddet al.

58 MaleH?

Rightoccipito-temporo-parietal

Cerebro-vascularaccident

Complex visual hallucinationsin both visual fields

Slowing of EEG on left, no mentionof seizures or of previouspsychiatric morbidity

[67]Medinaet al.

37 MaleRH

Leftoccipito-temporal

Infarct Complex visual hallucinations*in both visual fields agitationand aggressiveness

Slowing of EEG on left, agitationand aggressiveness

[67]Medinaet al.

42 MaleH?

Leftoccipital

Abcess Complex visual hallucinations*in both visual fields of people hehad seen before

No EEG, seizures or psychiatriccomorbidity mentioned

[68]Lunardiet al.

66 MaleH?

Rightoccipital

Abcess Complex visual hallucination*of objects (apparently in bothfields)


[69]Pattersonet al.

53 MaleRH

Rightoccipito-parietal

Glioblastoma Complex visual perseveration(palinopsia)* in both fields ofobjects seen over the previoushalf hour


[70]Maillotet al.

79 FemaleH?

Rightoccipital

Intracranialheamatoma

Complex visual hallucinations inboth visual fields


[71]Mukaetova-Ladinsket al.

47 FemaleH?

Rightoccipital

Infarct Complex visual hallucinations inboth visual fields


[72]Strandgaardet al.

68 MaleH?

Leftoccipital

Infarct Complex visual hallucinations*in both visual fields (central vision)


[61]Michel& Troost

66 MaleH?

Rightoccipital

Glioblastoma Complex visual perseveration(palinopsia)* in both visual fieldsof objects and people

Normal EEG, no psychiatriccomorbidity reported

[73]Lazaro


Table 1, continued


Locus ofthe lesion

Lesionetiology

Type of hallucination and locationin the visual field(s)* = the hallucinated image is fromepisodic memory


64 MaleRH


Ischemia Simple visual hallucinations(metamorphopsia) in both visualfields mild prosopagnosia

Slowing of EEG at posterior rightscalp, no psychiatric comorbidityreported

[32]Hoksbergenet al.

62 MaleH?


Infarct Simple vusual hallucinations“dazzle” in central fields


[74]Landiset al.

20 MaleH?

Leftoccipital

Penetratingwound

Simple visual hallucinations(polyopsia) in both visual fields

No EEG or seizures reported,personality and psychologicaltests failed to disclose significantneurotic trends

[75]Bender

56 MaleH?

Rightoccipital

Metastatictumor

Simple visual perseveration(palinopsia)* in both visual fields

Normal EEG, no mention ofseizures or of psychiatriccomorbidity

[76]Estefaniaet al.

tive paroxystic perilesional source of the hallucinationare in principle more interesting for a test of the psychictonus model than cases without EEG.

The ideal post lesion case for testing the psychictonus model would have a clearly unilateral lesionlimited to the occipital lobe (the visual cortex), on-ly one symptom (visual hallucination), the hallucina-tion would be complex, would contain elements fromepisodic memory, and would deploy in both visualfields, the patient would be right handed, he or shewould present no signs of seizures only slowing overthe lesion in EEG and no paroxysmal activity, and he orshe would not be too young nor too old. It is needlessto say that such perfect cases (for a test of the theo-retical model under consideration) of course are ratherrare. At any rate all these considerations are explicitlyaccounted for and regrouped accordingly in the nexttables -as far as the information was available in eachcase report.

Of the 78 cases of visual hallucination following aunilateral occipital lesion 48 (62%) had a right hemi-sphere lesion and 30 (38%) had a left hemisphere le-sion. A Chi2 test of probability indicates that this dif-ference is significant (Chi2 = 4.2, p < 0.043 two tailed)if one were to suppose that each hemisphere is equallyat risk for a lesion (see Tables 1, 2 and 3). These resultssupport the psychic tonus model.

We believe left and right hemisphere lesions indeedhave equiprobable chances of occuring and of beingselected for single case reports (in the absence of se-lection for type of visual disturbance). Duval andher colleagues [40] assembled 725 cases using simi-lar inclusion/exclusion criteria as here, except that theywere not selected for any particular cognitive or psy-

chiatric problem (an IQ test was required). This is thelargest such data base we are aware of. In that database there were 387 patients with left hemisphere le-sions and 338 with right hemisphere lesions (binomialprobability against equiprobability: p = NS, twotailed). Thus it can basically be assumed that when un-selected for memory disorder type, the two lesion sidesmay be considered theoretically equiprobable (or veryclose to that) when drawn from previously publishedreports.

3.2. Negative distortions of visual perception

Focal brain lesions can affect visual tonus negatively.The best example in the current story line would be aweakening of one’s ability to evoke a visual represen-tation from immediate memory. This loss of internalvisual evocation is none other than loss of the imagina-tive function, i.e., loss of imagination or “mind’s eye”.For purposes of replicability and clarity of our venturewe consider a pure loss of visual evocation in the awakemind as an inability to retain in short term memorya visual stimulus which could be properly describedand/or drawn in presence of the stimulus. This repre-sents something like the opposite of visual hallucina-tion. There are very few cases of this function beingselectively destroyed by a focal unilateral lesion. Somecases present signs of associative agnosia (problems ofverbal description of the object) or other aphasic signsor imperfect drawing of the object at copy.

We collected all previously published cases that wecould find of selective loss of visual imagery due to aunilateral lesion, specifically, loss of the ability to nonverbally evoke an image in immediate memory while


Table 2Non-paroxystic visual hallucinations limited to a single visual field following a radiologically or surgically objectified unilateral occipital lobelesion


Locus ofthe lesion

Lesion etiology Type of hallucination and locationin the visual field(s)* = the hallucinated image is fromepisodic memory


45 MaleH?

Leftoccipio-parietal

Meningioma Complex long lasting hallucina-tions, including palinoptic* in thecontralesional visual field


[77]Mooneyet al.

66 MaleM?

Rightoccipital

Infarct Complex visual hallucinations*in the contralesional visual field


[61]Michel& Troost

66 FemaleRH

Rightoccipital

Infarct +atrophy righttemporal

Complex visual hallucinationsin the contralesional visual field

EEG slowing over the lesion,no psychiatric comorbidityreported

[39]Kolmel

65 FemaleH?

Rightoccipital



[64]Lance

53 MaleH?

Rightoccipital



[64]Lance

73 FemaleH?

Rightoccipital



[64]Lance

72 MaleH?


Infarct Complex visual hallucinationsin the contralesional visual field

Normal EEG, no seizures orpsychiatric comorbidity reported

[64]Lance

74 FemaleH?


Infarct Complex visual hallucinations,including heutoscopic*, in thecontralesional visual field


[39]Kolmel

48 MaleH?

Leftoccipital



[64]Lance

64 MaleH?

Leftoccipital



[78]Benson& Rennie

56 MaleH?

Leftoccipital

Infarct Complex persistent visual halluc-inations in the contralesionalvisual field


[79]Kastenet al.

70 FemaleH?

Leftoccipital



[64]Lance

68 MaleRH

Leftoccipito-parietal

Oligodendro-glioma

Complex visual hallucinationsin the contralesional visual field


[39]Kolmel

50 FemaleRH


Resectedglioblastomamultiform

Complex visual hallucinationsin the contralesional field

No EEG or convulsion notedexcept once prior to resection, nopsychiatric comorbidity reported

[80]Freimanet al.

59 FemaleRH

Rightoccipital

Stroke Complex visual hallucinations,including palinoptic*, in thecontralesional field

Normal EEG (few independentsharp waves) no convulsionsmentioned, no psychiatriccomorbidity reported, righthypometabolism on SPECT

[35]Sun& Lin

64 FemaleRH

Rightoccipital

Resected tumoradenocarcinoma

Complex visual hallucinations*in the contralesional field

Absence of seizures is insistedupon by the authors but no EEGwas carried out, there were nohallucinations prior to resection,past history of anxiety and depr-ession

[81]Faber& Johnson

49 MaleH?


Excised tumor Complex hallucinations (persons,objects) in the contralesionalvisual field

EEG slowing over the lesion,no evidence of paroxysms, righthypermetabolism in SPECT

[26]Vogeley


Table 2, continued


Locus ofthe lesion



65 MaleH?

Rightoccipital

Arteriovenousmalformation

Complex visual hallucinationsin the contralesional field

EEG indicates no seizures,only supralesional slowing,no psychiatric comorbidityreported, SPECT indicatedright hypometabolismduring the hallucinations

[37]Inafukuet al.

73 FemaleH?


Infarct Complex visual hallucinations*in the contralesional field

No epileptic signs in EEG,phenytoin before and duringhallucinations did not preventthem, left hypoperfusion inSPECT

[82]Waragaiet al.

76 MaleRH

Rightoccipital

Infarct Complex visual hallucinationsin the contralesional field

No EEG or seizures mentioned,“no history of previous neurolog-ical or psychiatric disorders”

[83]Beniczkyet al.

72 MaleRH

Rightoccipital



[84]Cogan

84 FemaleH?

Rightoccipital

Meningioma Complex visual hallucinationsin the contralesional visual field


[85]Nagaratnamet al.

84 Female Rightoccipital

Stroke Complex visual hallucinationsin the contralesional field

No EEG, seizures or psychiatriccomorbidity mentioned, righthypometabolism on SPECT

[30]Assadiet al.

63 MaleRH

Leftoccipital



[86]Cole

? MaleH?

Leftoccipital

Stroke Complex visual hallucinations*in the contralesional visual field

No EEG, seizures mentioned,psychiatric tests were negative

[87]Anderson& Rizzo

33 MaleH?

Leftoccipital

Arteriovenousmalfrmation

Complex visual hallucinations(palinoptic)* in the contralesi-onal visual field


[88]Ritsema& Murphy

70 MaleH?

Rightoccipital

Infarct Complex hallucinations incontralesional field

No evidence of paroxysms inEEG, no psychiatric comorbidityreported

[89]Kompfet al.

50 maleH?

Rightoccipital

Infarct Complex hallucinationsin contralesional field


[89]Kompfet al.

62 MaleRH

Leftoccipital

Infarct Complex visual hallucinations,including palinoptic* in thecontralesional field


[90]Huna-Baron&Kupersmith

54 MaleH?

Leftoccipital

Infarct Complex visual hallucinationsin the ipsilesionalvisual field


[91]Manford&Andermann

79 MaleRH

Leftoccipital

Infarct Complex visual hallucinationsin the ipsilesional visual field

Normal EEG including duringhallucinations, “no personal orfamily history of psychiatricdisease or substance abuse”

[87]Anderson& Rizzo

82 FemaleRH

Leftoccipital

Infarct Simple visual hallucinations(diplopia) in the contralesionalfield


[90] Huna-Baron&Kupersmith


Table 2, continued


Locus ofthe lesion



50 MaleRH

Rightoccipital

Thrombosis Simple hallucinations and complexvisual perseveretion (palinopsia)of a few seconds in the contrale-sional visual field


[92]Ardilaet al.

64 FemaleH?

Leftoccipital

Infarct Simple hallucinations in contrale-sional field

Normal EEG with slowing overthe lesion, left occipital hypome-tabolism on SPECT, no psychia-tric comorbidity reported

[31]Flintet al.

37 FemaleH?

Rightoccipital

Metastaticcarcinoma

Simple hallucinations in thecontralesional field


[93]Johnson

35 MaleH?

Leftoccipital

Tuberculoma Simple visual hallucinations(palinopsia) in the contralesionalvisual field

No EEG seizures or psychiatriccomorbidity mentioned

[94]Werring& Marsden

84 FemaleH?

Leftoccipitl

Ischemia Simple long lasting hallucina-tions in the contralesional field


[24] Bosleyet al.

? FemaleH?

Leftoccipital

Etiology notspecified

Simple hallucinations in theipsilesional visual field

No EEG seizures or psychiatriccomorbidity reported

[87] Ander-son& Rizzo

22 MaleH?

Rightoccipital

Penetratingwound

Simple visual hallucinations(polyopia) in the ipsilesional field

No EEG seizures or psychiatriccomorbidity reported

[75]Bender

being able to describe and/or draw an object providedit is within visual reach. All the cases found had a leftoccipital lesion except the case of Riddoch [41] whohad a left temporo-parietal lesion. As far as we coulddetermine all these cases had lost visual evocation inboth visual fields. See Table 4.

All 12 cases of Table 4 had a left hemisphere lesion.The two tailed binomial probability of this occurringby chance is p < 0.0005. The profile strongly supportsthe psychic tonus model.

Most of the authors of these reports on loss of visualimagery are aware of the preponderance of left hemi-sphere lesions in loss of mental imagery. Most of theminterpret their patient’s loss as a verbal-imaginal prob-lem. They believe language, particulary its semanticaspect, contributes a “code” which consolidates imagesin memory [42]. They seem to hint that there mustexist a posterior module of language dedicated to thispurpose or that modules of imagery are disconnect-ed from those of language [12] -thus explaining whytheir patient is not aphasic outright. Several authorsdemonstrated that the patient could draw on copy butnot from immediate memory [12,41,43–45]. Farah andcolleagues [12] tested visual evocation likely to be to-tally unmediated verbally or semantically (pointing tothe color corresponding to that of an object presentedbefore) and indeed found a deficit. Several investiga-tions found a deficit of facial recognition (recogniz-

ing an unfamiliar face presented before) [12,46–48].This particular mental operation is probably not me-diated verbally or semantically. Several cases werenot aphasic at all. Three cases complained of havingstopped dreaming (the [12,46,49] cases). Despite this,commentators still clung to a verbal (more specificallysemantic) mediation concept of mental images to ex-plain the lesion locus and deficit of visual evocationof the patients in Table 4. Our psychic tonus modelproposes a different perspective on these cases. With-out denying that language may certainly contribute toevocability of mental images our model proposes thatthere is simply a paucity of mental representation as-sociated with activation of the intact right hemisphereand there is an exuberance of the same representationassociated with activation of the intact left hemisphere.This balance of hemispheric specializations affects lan-guage as much as any other aspect of mental life, ex-plaining why post lesion overtalkativeness (hyperlalia)is radically associated with right hemisphere lesions [3,50]. Thus left hemisphere lesions can be expected toreduce spontaneous expression and evocability of bothlanguage and mental imagery as well as any other cog-nitive content (except perhaps for contents for whichthe right hemisphere is radically specialized, but wethink there is no such thing).

Since visual hallucination and loss of visual imageryare two opposites, comparison of the 78 cases of oc-


Table 3Non-paroxystic visual hallucinations following a radiologically or surgically objectified unilateral occipital lobe lesion (location of the hallucina-tions in the visual fields unmentioned)


Locus ofthe lesion

Lesionetiology

Visual symptoms Clinical considerations Reference

40 MaleRH


Infarct Complex visual hallucinations ofobjects and persons (visual fieldnot specified)

No EEG, no signs of seizures,no psychiatric comorbiditymentioned

[95]Bhaskaran& Prabhu

82 MaleH?

Rightoccipital

Infarct Complex visual hallucinations(visual field not specified)


[96]Dejerineet al.

78 MaleH?

Leftoccipital

Infarct Complex visual hallucinations(visual field not specified)


[96]Dejerineet al.

56 MaleH?

Rightoccipital

Infarct Complex visual hallucinations(location unspecified)

Normal EEG, no mention ofseizures, no psychiatric comor-bidity reported

[97]Vaphiadeset al.

46 MaleH?

Rightoccipital

Infarct Complex visual hallucinations*(location unspecified)


[97]Vaphiadeset al.

46 FemaleH?

Rightoccipital


Right slow focus in EEG, nomention of seizures, no psy-chiatric comorbidity reported

[97]Vaphiadeset al.

72 MaleH?



EEG slowing on left side, nomention of seizures, no psy-chiatric comorbidity reported

[97]Vaphiadeset al.

60 MaleH?

Rightoccipital

Atheroma Complex visual hallucinations(of objects and persons)*location unspecified


[93]Johnson

32 FemaleH?

Rightparieto-occiptal

Infarct Complex visual hallucinations*(visual field not specified)


[98]Critchley

67 MaleRH


Hemorrhage Complex visual hallucinations(location unspecified)


[99]Ott& Saver

66 FemaleH?

Rightoccipito-parieto-temporal

Hemorrhage Complex long lasting visualhallucinations, prosopagnosia,topographical agnosia


[100]Dutton

71 FemaleH?

Leftoccipital



[97]Vaphiadeset al.

67 FemaleH?

Rightoccipital



[97]Vaphiadeset al.

62 MaleH?

Rightoccipital

Infarct Simple visual hallucinations(location unspecified)


[97]Vaphiadeset al.

46 MaleH?


Infarct Palinopsia, not furthercharacterised (locationunspecified)


[74]Landiset al.

46 MaleH?


Infarct Visual hallucinations (notfurther characterized norlocalized)


[93]Johnson


Table 3, continued


Locus ofthe lesion

Lesionetiology


35 MaleH?

Rightoccipital

Ischemia Visual hallucinations (nature not fur-ther specified, location unspecified)

No EEG, seizures or psychiatric co-morbidity mentioned

[101]Kanzakiet al.

42 MaleH?


Cysticlesion (unspeci-fied etiology)

Visual hallucinations palinopsia (lo-cation unspecified)

No mention of EEG, seizures or psy-chiatric comorbidity

[74]Landiset al.

Table 4Non paroxystic bilateral loss of visual imagery in the waking state following a unilateral occipital lesion

Age at onsetgender and handpreference

Locus ofthe lesion

Lesionetiology


19 FemaleH?

Leftoccipital

Closed headinjury

Loss of mental images, associ-ative agnosia, no aphasia

No EEG paroxysms or psychia-tric comorbidity mentioned

[48]Davidoff& Wilson

51 MaleH?

Leftoccipital

Closed headinjury

Loss of mental images, seman-tic access agnosia, no aphasia

No EEG, paroxysms or psychia-tric comorbidity mentioned

[45]Riddoch&Humphreys

56 MaleRH

Lefttemporo-occipital

Infarct Loss of mental images, visuo-imaginal constructional apraxia,no aphasia


[42]Grossiet al.

60 MaleH?

Leftoccipital

Infarct Loss of mental images, opticaphasia (partial loss of verbalaccount of mental images),aphasia limited to visualmediation


[102]Manning& Campbell

83 MaleRH


Infarct andhemorrhage

Loss of visual imagery, mildanomia without other signs ofaphasia


[44]Goldenberg

65 MaleRH


Infarct Loss of visual imagery, agraphia,Gerstmann syndrome, wordfinding difficulty


[103]Levineet al.

79 MaleH?


Infarct Loss of visual imagery, dyslexia,anomia, ipsilesional neglect


[104]Cocchiniet al.

63 MaleRH


Infarct Loss of visual imagery, alexiaand anomia for visuallypresented objects were the onlyaphasic signs, loss of dreaming


[46]Bassoet al.

64 MaleRH


Infarct Loss of visual imagery, noaphasia, loss of dreaming

EEG “mildly abnormal”, noparoxysms or psychiatriccomorbidity mentioned

[12]Farahet al.

47 MaleRH


Infarct Loss of mental images, opticaphasia, loss of dreaming, noaphasia


[49]Pena-Casanovaet al.

35 MaleRH

Lefttemporo-parieto-occipital

Resectedmeningioma

Loss of visual imagery,dysphasia


[43]Delevalet al.

43 FemaleRH

Leftparieto-occipital

Hemorrhage Loss of mental images, visualassociative agnosia, evolvingto optic agnosia


[47]Benke


cipital post lesion visual hallucination (all the cases ofTable 1) with the 12 cases of occipital post lesion lossof visual imagery (all the cases of Table 4) – for lesionside appears perfectly meaningful. The double crosseddissociation predicted by the psychic tonus model ishighly significant (Chi2 = 15.8 p < 0.0005).

3.3. Secondary control analyses (all the cases N =90)

At first glance the results reported above seem to bein total concordance with the hypothesis of the psychictonus model. Furthermore, the stronger lateralizationof the hypognosic group than the hypergnosic groupis also in accord with the literature reviewed in theintroduction. However several contaminating variablescould challenge our main result.

3.4. The locus of the lesion

Visual hallucinations (including palinopsia) and theloss of mental imagery are more often the result of anoccipital or temporal lobe lesion than lesions locatedelsewhere (see [51] for a review). In the current study,occipital damage was an inclusion criterion but damageelsewhere was not an exclusion criterion. It was there-fore thought useful to verify whether a lobar differencein lesion extension could explain the main finding ofa crossed interaction between lesion side and type ofvisual disorder (hypo/hypergnosia). The locus of thelesion was coded for each lobe (frontal, temporal, orparietal) separately because a combined analysis wouldhave violated the rule of independence of the replicatesand cases. We partialed out presence/absence of a le-sion in each lobe as well as volume of the lesion (num-ber of lobes lesioned) in partial correlation analysis be-tween lesion side and type of visual disturbance. Thecorrelation (interaction) remained significant in eachcase (Rp > 0.41, p < 0.0005).

3.5. Presence of aphasic symptoms

Presence of aphasic symptoms (anomia, dysphasia,aphasia, impaired oral comprehension) was of interestbecause of the well documented hemispheric special-ization of the left hemisphere for language (see [52]for a review). Presence/absence of aphasic symptomscould compete with the psychic tonus model. Suchan eventuality would require a caveat in our interpreta-tion of our main findings, or at the very least, statisti-cal partialing out of this variable’s effect in our test of

the main hypothesis. As we expected their were morecases with aphasic symptoms in the hypognosic group(5/12) than in the hypergnosic group (1/78) (Chi 2 =27.3, p < 0.0005). However the crossed interactionbetween lesion side and type of visual disturbance re-mained robust after partialing out of presence/absenceof aphasia (Rp > 0.38, p < 0.0005).

Several other variables were also tested for the even-tuality of providing an alternative explanation for thefinding of a crossed dissociation of left and right le-sioned cases as a function of type of visual disturbance.For example psychiatric comorbidity (psychosis or ma-nia) could be associated with visual hallucination [53]and not loss of imaginal evocation. A sampling bias ofetiology of the lesion is important to consider becauseirritative pathophysiology (ex: tumor) could cause ef-fects contrary to stable lesions such as CVAs. Anoth-er concern is that certain etiologies (ex: head trauma)comprise subtle diffuse damage thereby compromizingthe “lesion side” inference. A sampling bias of handwriting preference would be important because a sig-nificant proportion of left handers have inverted hemi-spheric specialization (at least for language). Age isof concern because juveniles are less hemispherical-ly specialized than adults and because the very elder-ly have diffuse brain atrophy and could thus present“noisy” lesion side characterization as well. A gendersampling bias is relevant to consider because in manyrespects women have less hemispheric specializationthan men [54]. Date of publication is pertinent becausediagnostic methods have improved over the decades,particularly due to the passage from CT to MRI scan-ning. However, the crossed interaction between lesionside and type of visual disturbance remained robust af-ter partialing out of all these variables (Rp > 0.40, p <0.0005). In fact, none the control variables mentionedabove, was significantly related to the interaction be-tween lesion side and type of visual disturbance.

3.6. More specific secondary control analyses(hallucination cases only N = 78)

3.7. Perilesional release

Occipitally lesioned cases often present with hemi-anopia. In the neurologic literature it is well knownthat visual hallucinations often occur in the defectivevisual field [55]. It is thus of interest to analyse theincidence of hallucinations in each visual field. Of the39 cases with hallucinations in a single field, 36 hal-lucinated in the contralesional field and only 3 in the


ipsilesional field (Chi2 = 27.9, p < 0.0005) indicatingstrong (though indirect) support for the idea accordingto which the source of the hallucination is perilesion-al (ipsilesional) release. Bosley and colleagues [24]provide a particularly interesting description of perile-sional hyperperfusion during unilateral visual halluci-nation: they illustrate a slim ring of hyperperfusionon SPECT all around the lesion. It is noteworthy thatunilateral hallucination is nearly always contralesionalwhether the lesion be in the left or right occipital lobe.

3.8. Contralesional release

Perilesional release, we think, could be independentof hemispheric specialization. After all, it is observedas a highly localized phenomenon –close to the lesion,and it probably generates only unilateral hallucinations(although that remains to be determined). The psy-chic tonus model does not contest perilesional release.Rather, it proposes that there should be more halluci-nating cases with right hemisphere lesions and it sup-poses that that preponderance would be due to con-tralesional release. What then, in the current data basewould be the evidence for contralesional release? First,with regard to EEG, there are 12 cases out of the grandensemble of 90 manifesting unilateral EEG slowing,and ten of the twelve cases had ipsilesional slowing.This is a profile compatible with contralesional release.In addition, in the cases with EEG (N = 24, overall), inwhom we are more certain that the source of halluci-nation was not perilesional paroxystic irritation, therewas a significant preponderance of right hemispherecases (Chi2 = 6.0, p < 0.015). Secondly, in the grandensemble of 90 cases here, there are six cases with uni-lateral hypoperfusion on SPECT, all ipsilesional. Thisis also compatible with contralesional release. Of thesesix cases, four (67%) had a right hemisphere lesion(NS).

We propose that it would be worthwhile to furtherinvestigate both eventualities, of perilesional hyper-metabolism and of ipsilesional hypometabolism, as afunction of presence or absence of hallucination, inone or both visual fields. We expect it will be foundthat the two types of mediation of hallucination occur,and even that each can occur in a same patient. Wealso expect that perilesional hypermetabolism will befound to be more locally distributed (around the lesion)and that ipsilesional hypometabolism will be found tobe more widespread, diffusing throughout most of thehemisphere.

3.9. Complexity of the hallucination

A visual hallucination can be either simple (seeingcolored spots flickering lights, etc., N = 13/78 caseshere) or complex (seeing a living scene, an animal, aperson etc., N = 62/78 cases here). The complexi-ty of hallucination, thus defined, was not significantlyassociated with lesion side. Whether the hallucinationsoccurred throughout both visual fields (N = 21/78) orwere restricted to only one field (N = 39/78) was un-related to lesion side. Finally, cases whose halluci-nation(s) included elements of episodic memory (el-ements highly specific to the patient’s history) (N =28/78) were not more likely to have right hemispherelesions than the cases without episodic memory content(N = 47/78).

4. Discussion

The results of this investigation support the psychictonus model. Unilateral occipital lesions causing a“positive” disturbance of visual representation (hyper-gnosia) are more often located in the right hemisphere.Unilateral occipital lesions causing “negative” distur-bance of visual representation (hypognosia) are alwayslocated in the left hemisphere of right handers.

Why would a focal left occipital lesion impair a pa-tient’s visual representation of the entire visual field?Such an effect cannot be attributed to damage of pri-mary sensory tracts. Primary visual representation hasbeen mapped in many species and has always beenfound to be strictly contralateral and to present thesame topography in each hemisphere in each occipitallobe, including in man [56]. Likewise, why would aright hemisphere lesion be more likely to provoke hal-lucinations in both visual fields? These are high or-der cognitive phenomena not explainable as direct neu-rosensory effects. We propose that the cerebral hemi-spheres influence higher level representation via psy-chic tonus regardless of the modality (motor, somat-ic, auditory, visual, immune, etc.). Psychic tonus maybe only one among several sorts of hemispheric spe-cialization, or it may eventually be made to fit into amore general and well integrated theory of hemisphericspecialization. Hemispheric specialization for psychictonus is a proposition that goes against the dominantneuroscience zeitgeist of today which is cognitivism.Psychic tonus is an unusual way of contemplating te-lencephalic and a fortiori cortical function. Uncon-scious and/or involuntary functions have more typical-


ly been conceived to depend on phylogenetically prim-itive brain tissue (e.g. the autonomic nervous system,the limbic system), and that might indeed be the case,but the lesion data indicate so far that psychic tonus isneocortically implemented in the human brain.

It could be thought that the main mediator of thepost lesion “sticky switch” is one or several neurotran-smitters. Three candidates are central norepinephrine,serotonin and dopamine (all known to modulate func-tions subsumed under psychic tonus). Robinson andcolleagues [57,58] ligated the middle cerebral arteryof rats. Assays of brain catecholamines revealed 30percent reductions of norepinephrine in the injured anduninjured cortex and locus coeruleus and a 20 percentreduction of dopamine in the substantia nigra in theright lesioned rats who had also become hyperactive.In contrast rats with left middle cerebral artery liga-tions did not become hyperactive and did not showany significant change in catecholamines in any of thebrain areas studied. Similar asymmetry occurs in sero-tonin concentrations as a function of stroke side in hu-mans [59]. It remains to be determined whether thelatter effect is hemispherically symmetrical or not (e.g.,a PET ligand study). In fact however we believe thatsuch a neurotransmitter-mediated mechanism is not theprincipal determinant of hemispheric specialization forpsychic tonus effects reported here and elsewhere. Su-perficial cuts in rat cortex modulate psychic tonus with-out affecting neurotransmitter concentrations [1], andictal visual hallucination results far more often fromleft foci [60]. This corroboration of hemispheric spe-cialization for psychic tonus cannot be explained as achronic and major change of neurotransmitter concen-tration in the brain after lesions. In other words, it ispresently best explained as true hemispheric special-ization, in the full sense.

Acknowledgments

This research was made possible by a grant from theFonds de Recherche en Sante du Quebec (FRSQ).

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