Dr Antonio Carota MD, Neurologist

The prosody is a communicative linguistic function, which results from the intonation, cadence, accent, and physical duration of the words. The prosody enhances the comprehension or the composed words, the basic emotions (rage, fear, sadness, surprise, disgust, pleasure), the subtle emotional aspects of the discourse (irony, sarcasm, deception, boredom, solace), and allows the differentiation of declarative, interrogative, and imperative phrases.

Thus, the expressive (affective) dysprosody is a suprasegmental deficit of language which should not be explained by a motor (dysarthria) or premotor (language apraxia) deficit, nor phonological or aphasic dysfunction (such as agrammatism and anomia). The patients with receptive dysprosody do not understand the emotional information of the phrases or the meaning of gesticulation.

Affective dysprosody could be an early predictor of post-stroke depression.Several studies on brain-damaged patients and normal subjects demonstrated the dominant role of the right hemisphere for prosody. In acute stroke settings, the assessment of dysprosody by bedside tests could help in localizing the lesion to the right hemisphere. Dysprosody, during epileptic seizures, has been linked to right hemisphere foci. The profile of anatomical correlation of prosodic syndromes (motor aprosodia for anterior and receptive dysprosody for posterior lesions) seems to parallel one of the aphasic syndromes of the left hemisphere.

Functional neuroimaging studies on normal subjects also provided a dichotomous scenario for linguistic functions such as the left hemisphere dominance for phonological and phonetic aspects versus the right hemisphere dominance for the emotional aspects.

Dysprosody might be amenable to behavioral treatments.

Apraxic agraphia is a very rare condition. The examiner should think about it when the patient shows normal linguistic capabilities (conversation is normal or almost normal) together with severely impaired writing. Apraxic agraphia is a peripheral writing disorder. Patients with apraxic agraphia have reduced ability to make the motor movements needed to write letters and sequence writting strokes. However, they usually have unimpaired capabilities of oral spelling. In the case of apraxic agraphia, writing is hesitant, imprecise and the disorder should not be explained by motor, sensory, extrapyramidal or cerebellar deficits and executive dysfunction (perseverations).
In case of stroke apraxic agraphia has been reported with frontal, parietal and thalamic lesions. Apraxic agraphia can manifest also with frontotemporal dementia and corticobasal syndrome.
Recently, I examined a 60 years old left-handed man, who had brain multiple ischemic stroke due to an hypercoagulability “trousseau’s syndrome”. The brain MRI showed 2 large lesions respectively of the left superficial territory of the posterior cerebral artery (occipital-temporal basal regions) and of the right parietal supramarginal gyrus.  Motor and sensory examination was normal.
This patient had normal linguistic output (normal conversation), mild denomination deficit, signs of visual apperceptive agnosia, alexia (letter-by-letter reading), and some features of apraxic agraphia. Oral spelling was spared. The patient’s writing was extremely low and hesitant as he did not remember how to do it.
An example of the patient’s writing on dictation is reported in the figure.
In this case, it is difficult to establish clinical-anatomical correlations (the same dysfunction is at the origin of both agraphia and alexia?), without further assessment but patients with atypical dominance could help in dissociating mechanisms of neurocognitive syndromes. Could you suggest your personal protocol to assess agraphia?

Eating disorders should raise up from dysfunction of neural processing in brain areas that are involved in emotional control, appetite regulation and body schema representations. In this context, eating disorders are located in the interface between the mind, body and the sense of self-agency.
It has been suggested that changes of the cognitive control exerted by the dorsolateral prefrontal cortex on the anterior ventral striatal pathway (a center predisposed to appetite regulation according to feelings of positive or negative reward) could trigger bulimic or anorexic behaviors.
One of the best evidence of such control cortical mechanisms on appetite regulation is the « Gourmand Syndrome » described by T. Landis and coll. Such a syndrome, which was identified in stroke patients with right hemisphere anterior lesions, consists of developing passion or manic thoughts for fine food and eating.
Even if the localizations and psychological mechanisms were globally known it would be still difficult to understand cortical changes in the brain in term of more specific circuits and neurotransmitters. To proceed to such a knowledge systematic studies with specific questionnaires or experimental cognitive eating paradigms (coupled with functional neuroimaging) should be conducted on patients with focal brain lesions or focal epilepsies.
Repetitive magnetic stimulation or transcranial direct current stimulation therapies, based on the result of those researches, would be tempted on patients (without brain lesions) and with eating disorders such as bulimia or anorexia or on patients with malnutrition or obesity

The frontal lobe is the main site of cognitive, emotional and behavioral processing. The prefrontal cortex, because of heavy bidirectional connections with all the other associative areas of the brain has long been assumed to have functions of control over other cognitive functions. This function has been termed
“executive”, meaning that rather than performing primary cognitive operations, such as memorizing, speaking and seeing, the frontal regions control the deployment of such capabilities, which are carried out elsewhere in the brain.
Therefore, the role of the frontal lobes is regarded as “supervisory” or “managerial” rather than being limited to the performance of any specific cognitive function. The frontal lobe is “the master and commander” of our brains. As per cognitive functions the frontal areas (as consistently demonstrated by fMRI studies) play a central role in working memory tasks. Working memory is the faculty that is responsible for the transient holding, associating and processing of new and already stored information, a fundamental process for reasoning, comprehension, learning and memory updating. Intelligent people or people gifted with the so called “fluid intelligence” generally have high capabilities of working memory.
As per the cognitive deficits patients with frontal lobe lesions show working memory deficits, poor logic and judgment, diminished sustained attention and mental speed, poor capacities of planning and organizing, poor abstraction, mental inflexibility, difficulties to control automatisms and task-switching,
The frontal lobes are the “master and commander” of emotional and behavioral processing too.
Evidence of the role of the prefrontal cortex in behavior and personality changes comes from the description of patients with frontal lobe damage. Such patients tend to be emotionally impulsive and poorly affectively regulated. Their behaviors include decreased concern with social propriety, environmental dependency, utilization, imitation and stereotyped behaviors, restlessness, exuberance, euphoria, facetiousness, extroversion, lack of restraint, purposelessness, childish behavior, distractibility, egocentricity, grandiosity, capriciousness and instability, social and sexual disinhibition, poor judgement, diminished foresight, social withdrawal, absence of tact, concreteness, acting on simple motivations, impulsiveness, self-centeredness, immorality, inertia, lack of ambition, indifference to the environment, satisfaction with inferior performance, slowness in thinking, bradypsychism, lack of emotional expression, decreased self-concern, shallow affect, depressed outwardly directed behavior and social sense, indifference, and alexithymia, lack of empathy and impaired theory of the mind (the ability to attribute mental states to others and to oneself), ritualistic or compulsive behaviors. Furthermore, several of these conditions may often occur together in the same patient.
Damasio and Stuss suggested that all behavioral and emotional changes due to frontal system damage might be a personality disorder where lack of control and self-reflectiveness (vulnerability to interference, impoverished judgment, and inability to self-correct and self-monitor) are the key features.
Hence, the DSM taxonomy of personality disorders (paranoid, schizotypic, antisocial, borderline, histrionic, narcissistic, avoidant, and obsessive–compulsive) seems to fit well with the so-called “frontal” behaviors.
The rehabilitation of the individual with a dysexecutive/frontal syndrome is a true challenge for the clinician and requires complex multidisciplinary approaches.