Psychology & Neuroscience
Some Rare Neuropsychological Syndromes: Central
Achromatopsia, Bálint’s Syndrome, Pure Word-Deafness,
Supplementary Motor Area Aphasia
Alfredo Ardila
Online First Publication, June 29, 2017. http://dx.doi.org/10.1037/pne0000093
CITATION
Some Rare Neuropsychological Syndromes: Central Achromatopsia,
Bálint’s Syndrome, Pure Word-Deafness, Supplementary Motor
Area Aphasia
Alfredo Ardila
Florida International University
There are some unusual neuropsychological syndromes rarely reported in neuropsy-chological literature. This article presents a review of four of these unusual clinical syndromes: (a) Central achromatopsia (loss in the perception of colors due to a lesion of the visual association cortex); (b) Bálint’s syndrome (simultanagnosia, optic ataxia and gaze apraxia associated with bilateral parietal-occipital pathology); (c) pure word-deafness (clinical syndrome characterized by an inability to understand spoken lan-guage with preserved speech production and reading ability); and (d) aphasia of the supplementary motor area (significant difficulty in initiating and maintaining speech, regardless if the patient makes significant effort to speak due to a damage in the left supplementary motor area). It is concluded that although these syndromes are rare, it is fundamental to consider them to understand the brain organization of cognition. Their understanding is also crucial in the clinical analysis of patients with brain pathologies.
Keywords:central achromatopsia, pure word-deafness, SMA aphasia, Bálint’s syndrome
There exist unusual neuropsychological syndromes that are rarely reported in the neu-ropsychological literature. A previous article analyzed somatoparaphrenia, akinetopsia, re-duplicative paramnesias, and autotopagnosia as examples of these unusual clinical syndromes (Ardila, 2016). In this article, central achroma-topsia, pure word-deafness, aphasia of the sup-plementary motor area (SMA), and Bálint’s syndrome will be reviewed. They are so rare, that they are not even mentioned in basic neu-ropsychology textbooks (e.g., Horton & Wed-ding, 2008); or barely one or two of them are briefly mentioned (e.g., Banich, 2004; Bau-mont, 2008; Elias & Saucier, 2006; Heilman & Valenstein, 2012; Kolb & Whishaw, 2015; Rains, 2001; Zillmer & Spiers, 2001). Indeed, only some of these syndromes appear in neuro-psychology dictionaries (Beaumont, Kenealy, & Rogers, 1999; Goodwin, 1989; Loring & Meador, 1999). Because of their rarity, from the
fundamental point of view, they have a special interest for understanding the brain organization of cognition. From the clinical perspective, they may be overlooked if we are not sufficiently aware of their existence.
In this article, two visual perceptual syn-dromes (central achromatopsia and Bálint’s syndrome) and two language syndromes (pure word-deafness and aphasia of the SMA) are analyzed.
Central Achromatopsia
Definition and Initial Description
Central (or cerebral) achromatopsia has been defined as a loss in the perception of colors due to a lesion of the visual association cortex (Damasio, Yamada, Damasio, Corbett, & Mc-Kee, 1980; Meadows, 1974). Total loss of color perception due to a brain pathology is a very unusual clinical syndrome, and as a matter of fact, only few cases have reported this(Ardila, 2009; Bartolomeo, Bachoud-Lévi, & De Schot-ten, 2014; Cowey, Heywood, & Irving-Bell, 2001; Crognale, Duncan, Shoenhard, Peterson, & Berryhill, 2013; Damasio et al., 1980; Fine & Parker, 1996; Jaeger, Krastel, & Braun, 1989; Kraft et al., 2014; Meadows, 1974; Mullin et al.,
Correspondence concerning this article should be ad-dressed to Alfredo Ardila, Department of Communication Sciences and Disorders, Florida International University, 11200 Southwest 8th Street, AHC3-431B, Miami, FL 33199. E-mail: ardilaa@fiu.edu
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2009; Rizzo, Smith, Pokorny, & Damasio, 1993; Shuren, Brott, Schefft, & Houston, 1996; Tanaka, Kitahara, Nakadomari, Kumegawa, & Umahara, 2002; Vaina, 1994; von Arx, Müri, Heinemann, Hess, & Nyffeler, 2010). Some-times, the loss is only partial (Kennard, Lawden, Morland, & Ruddock, 1995); in such cases, the color perceptual defects usually affect the recognition of some specific colors.
Anatomical Correlates
Cerebral achromatopsia has been associated with bilateral ventromedial occipital and tem-poral lesions (Ardila, 2009; Bartolomeo et al., 2014; Crognale et al., 2013; Damasio et al., 1980; Rizzo et al., 1993; Tanaka et al., 2002). Frequently, cerebral achromatopsia is related to temporo-occipital infarcts, which involve the lingual and fusiform gyrus (Fine & Parker, 1996; Jaeger et al., 1989; Kennard et al., 1995). Lesions are assumed to involve the ventral me-dial region of the occipital lobe, sometimes re-ferred as the “color center” of the brain (Bartels & Zeki, 2000; Lebrecht & Michael, 2011; Zeki, 1990).
Some Additional Studies
Some studies have shown the patient with central achromatopsia is capable of keeping the memory (imagination) of the colors, regardless the inability to perceive them (Shuren et al., 1996). As a matter of fact, the inability to get a mental representation of colors (meaning, knowing what colors are associated with which objects) corresponds more so to a color agnosia and not to an achromatopsia (De Vreese, 1991). Central achromatopsia is usually correlated with other syndromes, such as prosopagnosia (Ardila, 2009; Damasio et al., 1980; Vaina, 1994), agnosia and topographical amnesia (Ar-dila, 2009; Kennard et al., 1995), visual agnosia (Ardila, 2009; Rizzo et al., 1993). In other words, defects in depth perception and spatial localization of stimuli (Rizzo et al., 1993), and pure alexia (Damasio, & Damasio, 1986; Rizzo et al., 1993; Shuren et al., 1996).
Ardila (2009) reported the case of a 47-year-old man who presented a cerebral achromatop-sia associated with bilateral temporo-occipital infarcts, with a conservation of the imagination of colors (e.g., the patients easily and correctly answered the question, “What colors have the
national flag?”). Additionally, the patient pre-sented visual agnosia, he reported that “all the things looked alike”; for instance, he confuses a package of cigarettes with the TV control and was unable to recognize the streets around his house. When meeting a neighbor, he had diffi-culties recognizing her and could only identify her by her voice timbre. No defects in cranial nerves were found, but the patient reported he could only see tones of gray; no visual field defects were recorded; no motor or sensory defects were observed. Furthermore, the visual track was normal and no extinction with double visual stimulation was found. One week later, a significant recovery of achromatopsia and asso-ciated visual agnosia was found.
How This Syndrome Provides Further Insight Into the Brain
Evidently, this syndrome is crucial to under-stand the brain organization of visual percep-tion, particularly color perception.
Conclusion
Disturbances in color recognition or achro-matopsia can be due to both retina abnormali-ties, such as observed in Daltonism, and cortical pathology on central or cortical achromatopsia.
Bálint’s Syndrome
Definition and Initial Description
Bálint (1909) described a cortical syndrome characterized by, (a) “psychic paralysis of gaze,” in other words, difficulties in simultane-ously processing multiple items (simultanagno-sia); (b) “optic ataxia,” referring to deficits in visually guided limb and eye movements; and (c) “spatial disturbances of attention,” meaning defects in visual attention (gaze apraxia). As secondary to the attention impairments, the pa-tient also presented defects in estimating dis-tances; according to De Renzi (1982), these defects would be considered the fourth charac-teristic of this syndrome. Holmes (1918) de-scribed six similar cases, but included the fro-zen gaze phenomenon. This syndrome has been known as “Bálint’s syndrome” or “Bálint– Holmes’s syndrome.”
Simultanagnosiarefers to the inability to per-ceive more than one single object at the time.
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The term simultanagnosia was initially pro-posed by first Wolpert (1924) to describe a condition where the patient could see individual details of a complex scene, but could not grasp the overall meaning of the image.Optic ataxia
(misreaching to visual targets) refers to impair-ment in visually guided reaching moveimpair-ments; it is a defect in guiding a finger toward a target, in absence of motor or sensory defects. It is con-sequently an impairment in the direction and visual control of movements. Spatial distur-bances of attention(Gaze apraxia) refers to the patient’s inability to carry out voluntary eye movements and to keep the eyes fixed in a stimulus. Eye movements are somewhat ran-dom, and the patient has difficulties to look at a new stimulus.
Bálint’s syndrome is frequently associated with other disturbances, such as alexia without agraphia, visual agnosia, prosopagnosia, and visuospatial working memory defects (Ardila & Rosselli, 2007; Funayama, Nakagawa, & Suna-gawa, 2015). Noteworthy, patients with Bálint’s syndrome frequently behave as if they were blind.
Anatomical Correlates
Since the initial descriptions presented by Bálint and Holmes, it has been accepted that Bálint’s syndrome is observed in cases of bilat-eral lesions; in the majority of the cases, pari-etal-occipital pathology (e.g., Rousseaux, Dela-fosse, Devos, Quint, & Lesoin, 1986; Valenza, Murray, Ptak, & Vuilleumier, 2004). Seem-ingly, to have a complete Bálint’s syndrome with the three clinical signs, bilateral lesions are required (De Renzi, 1982). A partial or incom-plete Bálint’s syndrome can be observed with unilateral (usually left) pathology (Hécaen & Albert, 1978). This has also been observed in some specific pathologies such as Alzheimer’s disease (Mendez, Turner, Gilmore, Remler, & Tomsak, 1990) and Creutzfeldt–Jakob disease (Ances et al., 2004).
Some Additional Studies
Bálint’s syndrome has been considered as a particularly interesting clinical syndrome and different review articles of Bálint’s syndrome are currently available (e.g., Biotti, Pisella, & Vighetto, 2012; Chechlacz, & Humphreys, 2014; Mevorach et al., 2014).
In the neuropsychology literature, there is at least one case of rehabilitation of Bálint’s syn-drome (Rosselli, Ardila, & Beltran, 2001). The rehabilitation protocol included both visuoper-ceptual retraining and a functional program de-signed to provide rehabilitation in contexts that are meaningful to the patient. After 1 year of treatment, a second neuropsychological evalua-tion was carried out. It was found a significant improvement in terms of both objective testing and the return of an integrated and productive lifestyle.
How This Syndrome Provides Further Insight Into the Brain
Bálint’s syndrome represents one of the clin-ical syndromes which has most contributed to the understanding of visual and spatial percep-tion (De Renzi, 1982; Farah, 2004; Hécaen & Albert, 1978).
Conclusion
Regardless that Bálint’s syndrome was ported over a century ago, the number of re-ported cases remains low; but its significance in understanding visual/spatial perception and in-tegration has been particularly important.
Pure Word-Deafness
Pure word-deafness is an unusual clinical syndrome first described by Kussmaul in 1877, where a patient was unable to understand spo-ken language with preserved speech production and reading ability. He referred to this syn-drome as “reinen Wortaubheit” (which trans-lates as “pure word-deafness”). This syndrome is not equivalent to “word-deafness,” character-ized by the impairments in phoneme discrimi-nation, which can appear together with other language defects in Wernicke’s aphasia (Auer-bach, Allard, Naeser, Alexander, & Albert, 1982). Sometimes is has been named as “audi-tory verbal agnosia” (Ulrich, 1978), but most authors prefer it as the original term “pure word-deafness” (e.g., Ackermann & Mathiak, 1999; Denes & Semenza, 1975; Gutschalk et al., 2015; Jörgens et al., 2008; Poeppel, 2001; Takahashi et al., 1992; Wolberg, Temlett, & Fritz, 1990).
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There are some authors, however, who have proposed that “pure word-deafness” and “word-deafness” can be interpreted as variations of the same syndrome. Auerbach et al. (1982) sug-gested that there are two distinct subtypes of pure word deafness: (a) when the deficit is pre-phonemic and related to a temporal auditory acuity disorder and (b) as a form that is inde-pendent of a temporal auditory acuity disorder, and has a deficit in linguistic discrimination that does not adhere to a prephonemic pattern. The former would be associated with bilateral tem-poral lobe lesions, whereas the latter would be observed in cases of left unilateral lesions. In addition, the first form represents an appercep-tive defect, whereas the second is a disorder in phonemic discrimination and may be consid-ered a fragment of Wernicke’s aphasia. This distinction, however, has not really been explic-itly integrated into aphasia literature. Reviewing the published cases, nonetheless, effectively makes it seems that, in some cases, an auditory acuity prephonemic disorder could exist (e.g., in those cases due to mesencephalic lesions; Ki-miskidis et al., 2004; Vitte et al., 2002). Whereas in other cases, the defect seems to be a more exact phoneme discrimination impair-ment, as it was assumed in the original descrip-tion of the syndrome (Kussmaul, 1877). More-over, this condition is usually reported in cases of cortical temporal lesions (e.g., Rosati et al., 1982).
Most of the published cases of pure word-deafness are single case reports (e., g. Baddeley & Wilson, 1993; Gibbons, Oken, & Fried-Oken, 2012; Gutschalk et al., 2015; Jörgens et al., 2008; Kim et al., 2011; Notoya, Suzuki, Furukawa, & Enokido, 1991; Otsuki, Soma, Sato, Homma, & Tsuji, 1998; Praamstra, Ha-goort, Maassen, & Crul, 1991; Slevc, Martin, Hamilton, & Joanisse, 2011; Takahashi et al., 1992; Tanaka, Yamadori & Mori, 1987), and only occasionally the report of two cases (e.g., Hayashi & Hayashi, 2007; Shivashankar et al., 2001; Vitte et al., 2002). This paucity in reports is due to its rarity.
According to the original description pre-sented by Kussmaul (1877), the core distin-guishing characteristics are presented as a se-vere inability to understand spoken language with preserved speech production, discrimina-tion of natural sounds, and reading ability. Pa-tients with this syndrome have extreme
difficul-ties discriminating phonemic contrasts. As a consequence, they exhibit a profound speech perception deficit with subsequent auditory lan-guage comprehension impairment. Speech can be perceived as a whisper; or as if other people were speaking in a foreign unknown language. In many features, this problem compares with the altered speech perception of late bilinguals, unable to discriminate non-native phonemes (Feldmann, 2004). However, the patient can read and understand written language, demon-strating that the language disturbance is limited to the auditory perception of language pho-nemes. It must also be emphasized that speech production is preserved, and hence, the lexical, semantic and grammatical knowledge of the language are not impaired; it is only the pho-neme auditory perception.
Furthermore, the majority of word-deafness reported cases are due to lesions of the superior left temporal lobe including primary auditory area (Brodmann Areas 41 and 42; e.g., Auer-bach et al., 1982; Gutschalk et al., 2015; Stefa-natos, Gershkoff, and Madigan (2005)), sug-gesting a purely perceptual deficit, and hence, an auditory (verbal) agnosia. However, some additional localizations of the pathology associ-ated with this syndrome have been reported; Joswig, Schönenberger, Brügge, Richter, and Surbeck (2015) reported a case of pure word deafness, associated with a pineal germinoma on the inferior colliculi in a young patient. After percutaneous radiation therapy, the size of the tumor decreased significantly, but the audiom-etry demonstrated a complete regression of the auditory deficit. In addition, there are at least three additional cases of the syndrome caused by a mesencephalic lesion (Kimiskidis et al., 2004; Vitte et al., 2002). Hayashi and Hayashi (2007) studied two patients with pure word-deafness due to a subcortical hemorrhage in the left temporal lobe. There are also reports of pure word-deafness associated with bilateral(Ear-nest, Monroe, & Yarnell, 1977; Tanaka et al., 1987) or left unilateral temporo-parietal lesions (Sato, Yasui, Isobe, & Kobayashi, 1982; Slevc et al., 2011; Takahashi et al., 1992).
Pure word-deafness has also been reported in some particular clinical syndromes such as de-mentia, both in Alzheimer’s disease (Kim et al., 2011), and in frontotemporal dementia (Gib-bons et al., 2012)– and Landau-Kleffner syn-drome (Notoya et al., 1991; Stefanatos, 2008).
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Pure word-deafness has been reported as a sub-type of primary progressive aphasia (Otsuki et al., 1998; Jörgens et al., 2008).
Aphasia of the SMA
Definition and Initial Description
Brickner (1940) reported that electrocortical stimulation of SMA resulted in continuous per-severation. Penfield and Welch (1951) observed arrest of speech associated with stimulation of this cortical region. However, language distur-bances associated with SMA pathology were reported relatively late in the aphasia literature. Arseni and Botez (1961) reported speech dis-turbances caused by tumors of the supplemen-tary motor area. The specific clinical character-istics of this type of aphasia were later described by Rubens (1975, 1976); he studied two right-handed patients with evidence of major infarc-tion in the territory of the left anterior cerebral artery; according to Rubens, these patients pre-sented: (a) a significant dissociation between intact repetition and grossly disturbed spontane-ous conversational speech, (b) an absence of phonemic paraphasias, (c) a lack of speech in-hibition, and (d) relative preservation of con-frontation naming and comprehension. The au-thor points out that, despite the initially profound motor aphasia, spontaneous conversa-tional speech returned in two to three months. Later on, Jonas (1981) referred to the participa-tion of the SMA in speech emission.
Anatomical Correlates
The occlusion of the left anterior cerebral artery is the most frequent etiology of this apha-sia, but has also been reported in cases of tu-mors and traumatic head injury (e.g., Ardila & Lopez, 1984; Krainik et al., 2003). Speech is characterized by (a) an initial mutism lasting about 2–10 days; (b) later, a virtually total in-ability to initiate speech; (c) nearly normal speech repetition; (d) a normal language under-standing; and (e) absence of echolalia. A right leg paresis and right leg sensory loss are ob-served; a mild right shoulder paresis and Babin-ski sign are also found. Language recovery is outstanding and is usually observed during the following few weeks or months.
The SMA is a mesial premotor area involved in the ability to sequence multiple movements
performed in a particular order (Tanji & Shima, 1994). SMA participates in initiating, maintain-ing, coordinatmaintain-ing, and planning complex se-quences of movements (Alario, Chainay, Le-hericy, & Cohen, 2006); it receives information from the posterior parietal and frontal associa-tion areas, and projects it to the primary motor cortex (Kandel, Schwartz, & Jessell, 1995). SMA damage is also associated with slow re-action time (RT; Alexander, Stuss, Picton, Shal-lice, & Gillingham, 2007). It has been observed that activation of the SMA precedes voluntary movement (Erdler et al., 2000); therefore, it can be assumed that SMA plays crucial role in the motor expression of speech processing (Fried et al., 1991). Nonetheless, the SMA is located at some distance—and indeed far away—from the classic language area postulated by Dejerine (1914) and assumed in most anatomical models of aphasia.
It has been suggested that SMA has a close connectional relationship with the prefrontal cortex and plays a critical role in the update of verbal representations (Tanaka, Honda, & Sa-dato, 2005). Neuroimaging studies in humans have demonstrated that SMA is active not only when speaking, but also when performing di-verse cognitive tasks, such as spatial working memory (Jonides et al., 1993), verbal working memory (Paulesu, Frith, & Frackowiak, 1993), arithmetic tasks (Hanakawa et al., 2002), spatial mental imagery (Mellet et al., 1996), and spatial attention (Simon et al., 2002) activities.
Evidently, the SMA is a complex motor cor-tical area, not primarily a language related brain area. Its role in language seemingly refers to the motor ability to initiate and maintain voluntary speech production.
Some Additional Studies
In the neurological and neuropsychological literature there exist only few publications about this type of aphasia. Most often, they are single case reports (e.g., Ardila & Lopez, 1984; Masdeu, Schoene, & Funkenstein, 1978; Pai, 1999; Ziegler, Kilian, & Deger, 1997). How-ever, Freedman, Alexander, and Naeser (1984) described 15 patients with pathologies in the an-terior cerebral artery of the dominant hemisphere involving the SMA– even though they used the name “transcortical motor aphasia”–. They de-scribed the clinical characteristics as limited
spon-This
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taneous speech, intact repetition, normal articula-tion, and good auditory comprehension. Additionally, Krainik et al. (2003) studied 12 pa-tients with surgical resection of medial frontal lesions, and attempted to relate the occurrence of speech deficits to the specific surgical lesion of the SMA. Six of 12 patients presented speech disor-ders. The deficit was similar in all patients, con-sisting of a global reduction in spontaneous speech, ranging from a complete mutism to a less severe speech reduction, which recovered within a few weeks or months.
The following language characteristics are usually found (Ardila, 2014): spontaneous lan-guage is limited, but lanlan-guage understanding and language repetition are normal; there is a significant difficulty in initiating and maintain-ing speech, regardless of the patient’s signifi-cant effort to speak; reading aloud is defective but reading understanding is nearly normal; writing is slow and painstaking.
Legs have a motor representation in the me-sial aspect of the frontal lobe motor areas. Con-sequently, right leg hemiparesis represents the most important neurological abnormality; fre-quently, an extension of the pathology found toward the parietal lobe, and hence, some right leg sensory loss can also be observed.
How This Syndrome Provides Further Insight into the Brain
Aphasia of the SMA is rarely reported in neurological and neuropsychological literature. As a type of aphasia, SMA presents some spe-cial characteristics, (a) appears as a conse-quence of a lesion outside the classical language area (i.e., perisylvian area of the left hemi-sphere); (b) was reported late in the history of aphasiology; and indeed was systematically de-scribed only during the mid1970s; and (c) tends to present a rapid spontaneous improvement; this last characteristic may be the reason to account why it was overlooked for so long time. Noteworthy, when initially described, SMA was interpreted as a transcortical motor aphasia (Rubens, 1976), and that idea remained for some time (e.g., Alexander & Schmitt, 1980; Freedman et al., 1984), regardless of the signif-icant differences in location and clinical char-acteristics with the traditional transcortical mo-tor aphasia (Ardila & Lopez, 1984; Berthier, 1999; Goldstein, 1917). Currently, it has been
suggested that the aphasia of the SMA is some-what secondary or “peripheral” aphasia, impair-ing the mechanisms required to produce speech, but not the language itself (Ardila, 2010).
Aphasia of the SMA illustrates the complex overlap between language and motor processes, which has contributed positively to further our understanding about brain representation of lin-guistic processes.
Conclusion
Aphasia of the SMA represents an unusual clinical syndrome characterized by the distur-bance of initiating, maintaining, coordinating, and planning complex sequences of movements used in speech. It could be regarded as an apha-sic or as a motor syndrome.
General Conclusion
In neuropsychology—as in any clinical ar-ea—there are some unusual syndromes that are found very sporadically. But their rarity does not diminish their importance in the fundamental understanding about the brain organization of cognition, as well as in clin-ical analysis of patients with brain patholo-gies. The four clinical syndromes analyzed before illustrate this type of neuropsycholog-ical unusual syndromes.
In this article, two visual perceptual syn-dromes (central achromatopsia and Bálint’s syndrome) and two language syndromes (pure word-deafness and aphasia of the SMA) were analyzed. Regardless their scarcity, their contri-bution to the understanding of the brain organi-zation of visual perception and language has been enormous. It does not seem easy to under-stand the cerebral organization of visual percep-tion (including perceptual integrapercep-tion, spatial location of objects, and recognition of color features) without considering the two percep-tual syndromes analyzed in this article. It does not seem easy to understand brain language organization with regard both to its perception, as well as to its motor production without con-sidering the neurological bases of phoneme per-ception and motor speech control.
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Received January 26, 2017 Accepted May 29, 2017 䡲
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