Henry Olders, MD, FRCPC
Verdun, Quebec, Canada
2 Oct 1990
Effect of medication on negative symptoms
An NIMH double-blind, placebo-controlled study of the effects of antipsychotic withdrawal (four weeks drug-free) followed by four weeks’ treatment with fluphenazine HCl in 19 young patients with chronic schizophrenia showed that negative (as well as positive) symptoms exacerbated and then abated with treatment withdrawal followed by treatment (Breier et al, 1987)
Nonlinguistic vocal indicators of emotion
Certain emotions can be recognized by voice cues, even when extreme speech distortions have been applied (eg playing the tape backwards, whispering, low-pass filtering with a 500 Hz cutoff) (Scherer, 1979)
Scale for the Assessment of Negative Symptoms (SANS)
Studies in cultures other than North America (Moscarelli et al, 1987) of the Scale for the Assessment of Negative Symptoms indicate that the “negative” or “deficit” syndrome can be evaluated reliably and is internally consistent.
The SANS showed little difference between a group of negative schizophrenics and a group of depressed patients (Kulhara & Chadda, 1997), suggesting that the Bleulerian concept of “core symptoms” lacks specificity. If there are differences in nonlinguistic vocal indicators between schizophrenia and depression, the SANS is not able to detect them.
Defective hemispheric processing in schizophrenia
Evidence for some defect in processing of information which relates to hemispheric differences comes from the finding on MRI scans that schizophrenics have smaller corpus callosum areas as well as lower callosum-brain ratios (Rossi et al, 1989)
A study of longterm inpatient schizophrenics in rural Ireland found a consistent and highly significant association between oro-facial tardive dyskinesia, cognitive dysfunction or muteness, and flattened affect, suggesting a common neurological process (Waddington et al, 1987)
Diagnosis of psychopathology by voice analysis
Temporal lobe epilepsy
“Patients with olfactory hallucinations undergo respiratory changes” because one holds his breath if one smells something bad (Moses, 1954, p 33).
“The schizophrenic voice often has a typical monologue character – as if the partner in a conversation is not addressed at all. This phenomenon is caused by absence of appeal dimensions.
In true fear, mucous membranes become dry, the turbinates shrink, leading to an oral voice quality, without the warming touch of nasal resonance. The desire for distance, to be left alone, is expressed by complete elimination of nasal resonance. In schizophrenics one may find an oral voice, as these persons have no desire for real communication even though they may talk constantly, in monologues (Moses, 1954, p 51).
“In schizophrenics we find the following vocal symptoms:
1. Rhythm is prevalent over melody. A rhythmic repetition of vocal patterns is characteristic.
2. Registers are often separated: isolated head-register is used for long periods, often for days. The use of mixed registers probably accompanies temporarily successful communication.
3. Complete absence of melisms. This represents the inability of the patient to express appeal.
4. Decreased nasal resonance.
5. Melody is never “gliding” but always jumping in intervals, often without any correlation to content.
6. Mannerisms are used in histrionic excess. When such a patient uses the voice of authority, it is almost a burlesque of the voice of authority.
7. Accents are inappropriate to the content of his speech. This is part of a constantly repeated rhythmic pattern which is maintained in an almost compulsive way” (Moses, 1954, p 122)
Melody of voice is changed in depressed people. “One often hears marked minor key with a tendency to lower the pitch. Each impulse to lower is accompanied by decrease in intensity. It is as if the strain of maintaining a higher pitch is too much for the patient. Again the minor key would prevent greater strain” (Moses, 1954, p 61).
“Uniformity in speech is always a pathological symptom. It characterizes the genuinely depressed voice even when the uniformity is present only to a limited degree” Moses, 1954, p 74).
In his review, Scherer (1979) found no studies reporting abnormally low fundamental frequency for the speech of depressives. There was some indication that pitch range is reduced, and that pitch changes are stepwise rather than gliding. The well-known monotony of depressive speech was claimed by some authors to be due to frequent repetitions of stereotypic downward pitch contours. Other findings included: lower intensity, reduced dynamic range, lack of emphatic accents, and slow and halting quality. Voice quality has been variously described as nasal and throaty, flat and hollow, and dull.
“The voice of the manic-depressive patient reveals as the predominant factor complete absence of exaggerated rhythmic patterns. Instead the speech melody gains increased importance. In depressed periods the range shrinks, and is increased in manic phases (Moses, 1954, p 123).
Manic emotions result in comparatively large intervals between pitches of individual syllables (Moses, 1954, p 62).
“The nasal resonance is marked, giving to the voice a “warmer” feeling. The milody glides through the pitches, the intervals are hardly ever jumpy. Accents often have a more musical nature, while the dynamic character of the accent decreases” (Moses, 1954, p 124).
“Manic condtions express themselves vocally through uncontrolled intensities, extremely wide range which “stretches” registers, and highly dynamic accents oten accompanied by fast tempo of speech. There is no appeal through pathos or melisms, and no esthetic balance of the whole mosaic of acoustic dimensions” (Moses, 1954, p 124).
“Communication deviance is the measure showing the most consistent results in distinguishing parents of schizophrenics from comparison groups….Parents manifesting most communication deviance had offspring showing most cognitive disturbance (ie the group of non-paranoid schizophrenics)” (Rund BR, Blakar RM, 1986)
Kanner in 1942 described autism as an inborn defect in affective contact; “until recently it has been so much easier to study linguistic and cognitive development than “affective contact” that this vital dimension of personal social behavior has been neglected.” “Children with infantile autism, Pervasive Developmental Disorder, and dysphasia have severe disturbances of … nonverbal communication. … Disturbances of communication … underlie other observed deficits. … Few observers have systematically investigated nonverbal communication in preschool autistic children.” (Shapiro T, et al 1987)
Ross & Stewart (1987) report on two patients who suffered injury to the right opercula, resulting in motor aprosodia. However, they also exhibited pathological crying, an extreme nonvolitional affective display thought to be organized by the basal forebrain and temporal limbic system through bilateral descending pathways. Normally, such extreme displays are volitionally controlled; in these patients, it is hypothesized that loss of control was due to the interaction of two factors: damage to the right neocortical motor system and endogenous depression. In one patient, treating the depression with a tricyclic resulted in disappearance of the pathological crying (the other patient died).
Kolb & Taylor (1981) argue that techniques involving the naturalistic observation of behavior, which have long been used in the analysis of affective behavior in nonhuman species, can be applied to the study of cortical function in humans as well.
By analysing the content of a speaker’s speech, it has been shown that aspects of affective state, interpersonal style, and psychopathology can be inferred. Oxman et al (1988) showed that content analysis can also be used to classify patients into their respective diagnostic groups (somatization disorder, paranoid disorders, cancer, and major depression) with an accuracy which compares favorably with that done by psychiatric raters.
Beaumont & Dimond (1973) demonstrated that schizophrenics performed significantly worse than normals or psychiatric controls in matching shapes or letters flashed briefly, when the matching was across hemispheres. They interpreted this as pathology of articulation between the hemispheres.
Children are at risk of disorders of individuation and socialization if parents have communication disorders (Solana, 1988). This author compared the communication disturbances of parents of schizophrenic children to those of parents of severely mentally retarded offspring. Parents of schizophrenics showed more communication disturbances; parents of “in remission” patients more so than for chronic patients (ie patients for whom genetic and biological factors may be more important).
“Since the manipulation of fundamental frequency in tone languages, such as Mandarin Chinese and Taiwanese, is intimately tied up with word meaning, whereas in nontone languages, such as English, only the intent of words, not their semantic representation, can be altered by intonation , one is able to tease apart issues involving prosodic, acoustic-phonetic, and behavioral relationships” (Ross, 1988). Right-brain lesions in Mandarin speakers produce various types of aprosodias analogous to English speakers without affecting tone production or precipitating tone aphasias (Hughes et al, 1983). Thus, “language functions are lateralized according to the behavior itself, eg affective vs linguistic” (Ross, 1988).
Effect of emotion on voice
Voice resonance is subject to emotions; the nasal mucous membranes, especially the turbinates, become engorged during sexual arousal, as well as during other emotional states and the recollections of emotional states (Moses, 1954) (p 50). Since nasal resonance depends on resonator space and the humidity of the tissues, emotional states are reflected in voice quality.
Melody in voice conveys meaning, even when no words are used (contrast the infant’s cry of command with a piteous wail) (Moses, 1954)
Experiments with simple invertebrates such as the simple mollusc Aplysia show that they are capable of learning by both non-associative and associative means, and that these different learning processes all give rise to short- and long-term memory (Kandel et al,1986). Serotonin and other transmitters released by facilitating neurons acting on the presynaptic terminals of sensory neurons activate a transmitter-sensitive adenylate cyclase in the membrane of the presynaptic terminal of the sensory neuron that increases the level of intracellular cyclic AMP, which then activates a protein kinase that phosphorylates a K+ channel protein, or a protein that is associated with it. This phosphorylation reduces one of the K+ currents that normally repolarize the action potential. Reduction of these currents prolongs the action potential and allows more Ca2+ to flow into the terminals. Protein phosphorylation also modulates the handling of Ca2+ within the sensory neurons and consequently more transmitter can be released. Closure of a K+ channel can have two quite different functional consequences: one, by enhancing the duration of the action potential, it can increase transmitter release presynaptically; two, by removing a conductance that acts both as a shunt of excitation as well as a hyperpolarizing force in the sensory neurons, it can decrease the threshold for spike initiation and counteract the tendency for accommodation during prolonged physiological or constant current stimuli.
Long-term facilitation is dependent on protein synthesis, and acts on the same locus as short-term memory. It may utilize genes and proteins not involved in short-term memory. Studies in culture indicate that repeated action of 5-HT can initiate long-term facilitation of the connection between the sensory and motor neurons. This suggests that the long-term process could arise from the repeated action of modulatory transmitters released by the short-term process.
Beaumont JG, Dimond SJ. Brain disconnection and schizophrenia. Br J Psychiatr 1973; 123: 661-2
Breier A, Wolkowitz OM, Doran AR et al. Neuroleptic responsivity of negative and positive symptoms in schizophrenia. Am J Psychiatry 1987 Dec; 144(12): 1549-55
Hughes CP, Chan JL, Su MS. Aprosodia in Chinese patients with right cerebral hemisphere lesions. Arch Neurol 1983 Nov; 40; 732-6
Kandel ER, Klein M, Castellucci VF, et al. Some principles emerging from the study of short- and long-term memory. Neurosci Res 1986; 3: 498-520
Kolb B, Taylor L. Affective behavior in patients with localized cortical excisions: role of lesion site and side. Science 1981; 214: 89-91
Kulhara P, Chadda R. A study of negative symptoms in schizophrenia and depression. Compr Psychiatry 1987 May/Jun; 28(3): 229-35
Moscarelli M, Maffei C, Cesana BM, et al. An international perspective on assessment of negative and positive symptoms in schizophrenia. Am J Psychiatry 1987 Dec; 144(12): 1595-8
Moses P. The voice of neurosis. New York: Grune & Stratton, 1954
Oxman TE, Rosenberg SD, Schnurr PP, Tucker GJ. Diagnostic classification through content analysis of patients’ speech. Am J Psychiatry 1988 Apr; 145(4): 464-8
Ross ED, Stewart RS. Pathological display of affect in patients with depression and right frontal brain damage. J Nerv Ment Dis 1987; 175(3): 165-72
Ross ED. Prosody and brain lateralization: fact vs fancy or is it all just semantics? Arch Neurol Mar; 45: 338-9
Ross ED. The aprosodias: functional-anatomic organization of the affective components of language in the right hemisphere. Arch Neurol 1981 Sep; 38: 561-9
Rossi A, Stratta P, Gallucci M, et al. Quantification of corpus callosum and ventricles in schizophrenia with nuclear magnetic resonance imaging: a pilot study. Am J Psychiatry 1989 Jan; 146(1): 99-101
Rund BR, Blakar RM. Schizophrenic patients and their parents: a multimethod design and the findings from an illustrative empirical study of cognitive disorders and communication deviances. Acta Psychiatr Scand 1986; 74: 396-408
Scherer KR. Nonlinguistic vocal indicators of emotion and psychopathology. In: Izard CE, ed. Emotions in personality and psychopathology. New York: Plenum Press, 1979
Shapiro T, Frosch E, Arnold S. Communicative interaction between mothers and their autistic children: application of a new instrument and changes after treatment. J Amer Acad Child Adol Psychiatr 987; 26(4): 485-90
Solana RM. Communication disturbances in parents of schizophrenics. Acta Psychiatr Scand 1988; 77: 427-34
Waddington JL Youssef HA, Dolphin C, Kinsella A. Cognitive dysfunction, negative symptoms, and tardive dyskinesia in schizophrenia: their association in relation to topography of involuntary movements and criterion of their abnormality. Arch Gen Psychiatry 1987 Oct; 44: 907-12
- Negative symptoms in schizophrenia
- Minor tranquilizers