Neurological Disorders

beginning with the letter...


The clinical study of aphasia began in 1861 with the observations of Paul Broca and Marc Dax and expanded upon by Dr. Wernicke.  Today we divide aphasia into 8-9 distinct syndromes based on language output, comprehension, repetition and naming.  There are criticisms for using this approach to classify different syndromes, but it does have it’s value when trying to describe patients. (Feinberg & Farah, 2003)



Despite reasonable clinical validity, these syndromes have at least four limitations.  First, they are polytypic (contingent upon several criteria).  Secondly, the syndromes are not stable even when the anatomy is.  Third, there is no certainty that signs all have the same pathology.  Finally, signs are dichotomous, impaired or not.  This simplification of impairment often is not amenable to more complex questions.  Despite the forementioned limitations, these syndromes do have utility.  They serve as shorthand for clinical communications. about pathology, prognosis and level of impairment.



Directly below is a flow chart followed by descriptions of the different syndromes.



                                                       Aphasia






                                 Non-fluent                                    Fluent




                    Poor                  Good                      Poor                   Good


           Comprehension   Comprehension   Comprehension   Comprehension




     Poor        Good         Poor         Good         Poor          Good        Poor          Good


Repetition Repetition Repetition Repetition Repetition Repetition Repetition Repetition





Broca’s Aphasia


This is a non-fluent aphasia which can be further categorized as (Chronic Broca’s Aphasia, Acute broca’s Aphasia, Broca’s Area Lesions or Lower Motor Cortex Lesions.)  Common symptoms include effortful, delayed production of speech and pronounced hesitation.  This condition can also be characterized by agrammatism, paragrammatism, dysprosody, dysarthria and hypophonia. (Feinberg & Farah, 2003)  All symptoms may not be present.


(e.g. “Son is throw ball.  Arm down! Oh boy! Okay Awright.  Okay..Ball is down...fall, and boy, okay,...boy...um”)



Wernicke’s Aphasia


Werincke’s Aphasia is a posterior fluent aphasia characterized by deficits in comprehension and naming.  Phonemic paraphasias, neologisms and cirumlocution are often present, Apraxia to command, phonemic paraphasias and right hemi-neglect also can be present. Fluent, well articulated, normal rate and intonation, semantic and phonemic paraphasias, paragrammatisms, poor comprehension.  More severe cases might have neologisms.





Conduction Aphasia


Identified by Wernicke, this is a fluent aphasia in which comprehension and fluency are intact, but repetition is impaired.  Limb ideomotor apraxia is common initially but clears in most patients. (2003, p 152)






Global Aphasia


These patients have significant impairment in all major language areas, but it is not jargonaphasia.  “The language comprehension tasks most likely to be preserved in global aphasia are pointing to a named location on a map, pointing to personally highly familiar names from multiple choice or acknowledging them when they are resented auditorily, and a small subset of commands (“take off your glasses,” “close your eyes,” “stand up”). (2003, p. 153)  The entire perisylvian region is usually afflicted.




Transcortical Motor Aphasia


Transcortical aphasias are the “linguistic opposite of conduction aphasia.”  (2000, p.62)  repetition is spared but other areas of language are disrupted.  In transcortical motor aphasia This condition often begins with mutism which leads to deficits in language output, initiation of speech and phrase length.  Sometimes fragmented echolalia is observed.n  The classic patient has a large dorsolateral frontal lesion extending deep into the frontal white matter.




Anomic Aphasia


The only language defects are word-finding difficulty and an inability to name objects on confrontation.  “Lesions in many parts of the dominant hemisphere can cause anomic aphasia; thus, the localizing significance of this type of aphasia is limited.” (Strupp & Black, 2000, p.63)  “The most severe anomic aphasia, however, is noted in patients with temporal lobe lesions involving the second and third temporal gyri.” (2000, p.63)  However, it can also accompany lesions to the angular gyrus.





Transcortical Sensory


This syndrome is consists of impairment in all areas except repetition.  These patients are often mute initially.







Mixed Transcortical


This condition is characterized by impaired comprehension, naming and fluency but intact repetition.



Pure Word Deafness


production may be normal


Poor comprehension


better recognition of environmental sounds




Everyone who takes the WAB get’s calssified, not just good Wernicke’s and good Broca’s examples





Feinberg, Todd, E, & Farah, Martha, J,,  Behavioral Neurology  Neuropsychology (Second Edition) New York, McGraw-Hill, 2003,



a range of impairments in the use of language that are caused by injury of damaged function in the perisylvian region of the dominant hemisphere



dyslexia


dysgraphia


arcuate fasciculus model isn’t true anymore, just a classical model



Aphasia types evolve a lot during recovery and severity lessens.  Evolution is related to the lesion site and patients that may appear similar acutely may evolve differently depending upon the damage.






Non-fluent (symptom)


dysartria


motor control problems


imprecise articualtion


consistent erros



Apraxia of speech


difficulty with motor planning


lexical accceess is relatively fgood


errors at the sonund level



Trancortical motor aphasia


brocao like output


ecolalai


good repetition






















                                                        Aphasia






                                 Non-fluent                                    Fluent




                    Poor                  Good                      Poor                   Good


           Comprehension   Comprehension   Comprehension   Comprehension




     Poor        Good         Poor         Good         Poor          Good        Poor          Good


Repetition Repetition Repetition Repetition Repetition Repetition Repetition Repetition



The clinical study of aphasia began in 1861 with the observations of Paul Broca and Marc Dax and expanded upon by Dr. Wernicke.  Today we divide aphasia into 8-9 distinct syndromes based on language output, comprehension, repetition and naming.  There are criticisms for using this approach to classify different syndromes, but it does have it’s value when trying to describe patients. (Feinberg & Farah, 2003)



Despite reasonable clinical validity, these syndromes have at least four limitations.  First, they are polytypic (contingent upon several criteria).  Secondly, the syndromes are not stable even when the anatomy is.  Third, there is no certainty that signs all have the same pathology.  Finally, signs are dichotomous, impaired or not.  This simplification of impairment often is not amenable to more complex questions.  Despite the forementioned limitations, these syndromes do have utility.  They serve as shorthand for clinical communications. about pathology, prognosis and level of impairment.



Directly below is a flow chart followed by descriptions of the different syndromes.







Aphasia