Juan P. Recagno Cepeda

Aphasia is called a language disorder. The aphasic patient uses his language incorrectly or has difficulty understanding it.

Aphasia should not be confused with dysarthria. A dysarthric patient poorly articulates words, but his grammar and word choice is correct. Dysarthria can originate from central or peripheral neurological lesions that affect the respiratory muscles that expel the air, the vocal cords, the motility of the tongue, the palate, the lips and the jaw, and the passage of air through the larynx, mouth and the nose.

All these peripheral mechanisms that intervene in the correct pronunciation are in turn controlled by the brain through corticobulbar connections, with the facial, trigeminal, glossopharyngeal, pneumogastric and hypoglossal nuclei and coordinated with the cerebellum. Therefore, various disorders of the articulation of the word (dysarthria) can be caused by central lesions of the corticobulbar pathways (pseudobulbar paralysis) or cerebellar, and by peripheral lesions of the cranial nerve nuclei mentioned IX, X and XII ( bulbar paralysis). Only the repeated experience of hearing the patient speak with these various types of injuries will allow the clinician to identify them, so it is unnecessary to describe them.

Aphasias, on the other hand, are almost always the result of an injury to the cerebral cortex in the left hemisphere, although the injury may sometimes lie immediately below the (sub-cortical) cortex.

Three exceptions to this general rule can be made: 1) around half of the left-handed patients can present aphasias with lesions of the right hemisphere; 2) nominal aphasias (simple difficulty in finding the name of an object, or how to say “have the word on the tip of the tongue”) can be caused by a metabolic disorder (hypoglycemia, for example) or by brain compression at a distance (tumor, for example) and in these cases there will be no injury to the left hemisphere; and 3) some lesions of the thalamus can produce aphasia.

These three exceptions are rare, for which reason it is very important for the clinician to identify an aphasia since then he will be able to say, with great probability of success: 1) that the patient has a cortical or subcortical organic lesion; 2) that this lesion is in the left hemisphere, and 3) that it is in the vicinity of Silvio's fissure (on his front or temporal lip). These cortical areas are supplied by the middle cerebral artery.

Within this wide corticosubcortical zone that surrounds the Silvian valley in the left cerebral hemisphere, an area historically described by Broca, located in the posterior portion of the third frontal gyrus, and an area described by Wernicke, located in the posterior portion of the first temporal gyrus, in the vicinity of the primary projection area of ​​the auditory pathway. Both areas are connected to each other by a bundle of white matter called an arcuate or arciform fascicle.

Vascular, tumor, traumatic, infectious or degenerative lesions of these areas and fascicles of the left cerebral hemisphere will give rise to a language disorder, which is called aphasia.

Aphasic patients can start their symptoms abruptly or slowly gradually, depending on the nature of the injury.

If this lesion is located in the frontal areas (de Broca) it will produce a predominantly expressive aphasia, also called Broca's aphasia. The word is slow and difficult, as of telegraphic type (omission of conjunctions, and terminations). The patient will be able to repeat single words, but not longer sentences, and will have difficulty naming objects that are pointed to. The writing will express the difficulties already observed in the spoken language. The patient recognizes his problem and errors and tries unsuccessfully to correct them. Due to their proximity to the cortical areas of the fine movements of the arm and hand, these patients suffer from a right hemiplegia with a predominance of the faciobrachia. Despite these difficulties in the expression of spoken and written language, you will be able to understand, instead, spoken or written language.

If the lesion is located in the temporal or Wernicke area, the disorder will be characterized by a fleeting language, with normal articulation and rhythm, but which transmits a message that is difficult to interpret due to the incorrect use of words. This is receptive or Wernicke's aphasia.

These paraphasic errors are not recognized by the patient, so the result is a language 4 that resembles jargon and that is sometimes confused with a mental disorder; and also unfortunately sometimes leads to an emergency admission to a psychiatric institution. This image is reinforced by the patient's inability to understand what is spoken or written, as if it were a foreign language. His calligraphy is good, but both what he writes and what he speaks do not make much sense. The patient may, at first, not recognize his deficit and not be frustrated by his difficulty in communicating. Hemiplegia may or may not be mild, but it may be a homonymous right quadrantopsia or hemianopia.

These two types of aphasia will not always present with well-defined characteristics in a particular case, for easy to understand pathophysiological reasons. Thus, for example, a large ischemic infarction in the territory of middle cerebral artery can produce a global aphasia in which the deficit completely prevents the patient from communicating with language.

Very small cortical lesions in the vicinity of the Wernicke area (angular gyrus) or metabolic or toxic alterations (drugs) of the brain, may have a minimal expression in the so-called nominal aphasia, previously mentioned, which lacks an accurate locator value with respect to the language areas.

The diagnosis of aphasias is, as follows from the preceding description, quite difficult for the inexperienced observer. It cannot be carried out by any other auxiliary or instrumental method and constitutes a whole field of neurological specialization that participates in psychoneurology and linguistics.

Phisycal examination

  1. The first is to be sure that the patient is fully conscious so as not to confuse a confusional state with an aphasia.
  2. There should be listen to how the words “come out”. Do they flow well or with difficulty? If they are fluent, the lesion is more posterior, if they are not, it is more anterior.
  3. Can the patient read and write without difficulty? If possible, he is not aphasic.
  4. Is there a hemiparesis? If there is, the injury is anterior with participation of the motor area.
  5. To separate the different types of fluent aphasias (with subsequent injury), see if the patient can repeat simple sentences, understand simple orders or name objects that one points out: a) if the injury is cortical, he will have difficulty in the three tests; b) if you can understand but cannot repeat or name objects, the lesion is subcortical or connecting (arcuate fascicle); c) if he only has difficulty naming objects (he recognizes them, but “he has the word on the tip of his tongue”), there will be a nominal aphasia, the locator value of which is lower (toxicometabolic disorders or injuries that exert pressure at a distance).

Recognizing an aphasia has great locator value. A patient with paresis or tingling of his right hand may have an injury to the brachial plexus or its branches, but if he also has aphasia, the injury will be left hemispherical. By far, this lesion is more often vascular and its cause should be sought from the heart (source of emboli) through the carotid in the neck (also source of emboli) and reaching the middle cerebral artery (eventual thrombosis). If the aphasia is abruptly installed and without hemiplegia, the 1st embolism is the most likely cause. Angiographic study often allows to identify the cause and proceed to its prevention.


When a lucid and cooperative patient, who does not suffer from paralysis or sensory deficits, cannot correctly perform a complex intentional movement (lighting a match, putting on the coat, using the cutlery), he is said to have apraxia. Like the aphasic patient, the condition can be mistaken for a mental disorder. However, the apraxic is aware of its difficulty, repeatedly tries to overcome it and appears frustrated by not succeeding. Apraxias are often associated with aphasias and, like these, they express organic injury at high cortical or subcortical levels (disconnection of one brain area from another).


If a patient does not have a sensory deficit that prevents him from picking up a visual stimulus (scotoma, hemianopia) and does not recognize familiar objects, he is said to be suffering from visual agnosia. If the same happens when you try to recognize an object by touch (looking for a key in your pocket, for example), you are talking about tactile agnosia.

Agnosias also have locator value and point to cortical or subcortical levels. These lesions are usually vascular in nature and located in the vicinity of the primary projection areas of the affected function (occipital lobe in visual agnosia, parietal lobe in tactile agnosia).