Disorders Of Skilled Movement Not Caused By Weakness

Apraxia Disorders of skilled movement not caused by weakness, deafferentiation (loss of sensory capacity), abnormality of tone or posture, abnormal movements, intellectual deterioration, poor comprehension, or uncooperativeness

Lashley’s Serial Order of Behavior Problem
The "only strictly physiological theory" to have been explicitly formulated was associative chaining theory, in which it is postulated that each element in a series of actions provides the excitation of the next.
But speech and piano playing is too fast.
Lashley postulated instead that the production of serial behaviour involves the parallel activation of a set of actions, which together comprise some "chunk", so that responses are internally activated before being externally generated. This activation, in itself, does not contain the serial ordering of the actions. Superimposed on this activation is some kind of independent ordering system, a "schema for action", which selects which response, of those activated, to produce at which time. Unfortunately, Lashley was able to progress no further, writing that,
“ ... that elements of the [sequence] are ... partially activated before the order is imposed upon them in expression suggest that some scanning mechanism must be at in regulating their temporal sequence. The real problem, however, is the nature of the selective mechanism by which the particular acts are picked out in this scanning process and to this problem I have no answer. “

The Muscle Spindle
Muscle spindles are found within the belly of muscles and run in parallel with the main muscle fibres. The spindle senses muscle length and changes in length. It has sensory nerve terminals whose discharge rate increases as the sensory ending is stretched. This nerve terminal is known as the ANNULOSPIRAL ending, so named because it is composed of a set of rings in a spiral configuration. These terminals (shown in blue) are wrapped around specialised muscle fibres that belongs to the muscle spindle (INTRAFUSAL FIBRES) and are quite separate from the fibres that make up the bulk of the muscle (EXTRAFUSAL FIBRES) .

Early Descriptions of Apraxia
Steinthal (1871) called it "apraxia"
Hughlings Jackson (1886) described
Liepmann & Maas (1907)
Because language mediated by left hemisphere
Because distal movements of left arm controlled by right motor cortex
Corpus Callosal damage disconnects language area from right motor area = patient cannot carry out motor commands with left hand.
His imitation was poor
When object was placed in his hand performance was poor
Patient was aware of poor performance
Since he could not imitate Liepmann and Maas proposed that the left hemisphere contains "skilled motor engrams" necessary for skilled movement

Liepmann : IDEOMOTOR APRAXIA
Inability to perform acts to verbal commands, even though they might be performed spontaneously, or when aroused emotionally
An example of one of his cases:
A man with left hemisphere stroke tried to complete commands with his left hand. Could not though it was not paralyzed (as right hand).
Right-handed patients with right hemisphere stroke did not show apraxia with their right hands.
Liepmann’s explanation:
left hemisphere was the “organizer” for skilled movements
suggested supramarginal gyrus of parietal was necessary = a patient with the corresponding section of the corpus callosum damaged also showed left hand apraxia.
HOWEVER: there are several cases studies in the literature (Gazzaniga, Geshwind) in which patients with callosal damage cannot perform to command but can imitate.
RH motor control still present: THEREFORE = something in left hemisphere is cut off – some skilled motor organizing thing Therefore they have both parts: control & skilled system (and it must be in left h.) Suggesting a disconnection of verbal and visual routes

Motor Engram Paralyzed hand Apraxic Hand Therefore

Motor Engram Paralyzed hand Therefore No engram here

Motor Engram Paralyzed hand Therefore No engram here Ipsilateral side must need the left-side engram

In 1905 Liepmann reviewed 83 cases classified as right or left damaged on the basis of the side of hemiplegia. The syndrome of apraxia occurred in about half of the right hemiplegics with left hemisphere damage.

Heilman K, Van Den Abell T. 1979. Right hemisphere dominance for mediating cerebral activation. Neuropsychologia 17: 315-21

1.Koskia, L., M. Iacobonia, and J.C. Mazziottaa, Deconstructing apraxia: understanding disorders of intentional movement after stroke. Current Opinion in Neurology, 2002. 15 : p. 71-77. Controversial: Ideational may be a severe form of ideomotor apraxia

Ideational Apraxia
And, “ideational apraxia” in which the patient identifies the wrong overall plan, despite preserving the elements. A common example is a patient who puts the match to their mouth to light with a cigarette in their hand. (large diffuse lesions and many question whether its not a severe form of ideomotor apraxia).
Some authors suggest that “pantomiming” tasks versus “imitating” tasks separate these two disorders, ideational apraxics failing on pantomiming but not imitation, and ideomotor apraxics on both - but this is also consistent with the idea that ideomotor is just more severe.
Assuming two syndromes - then ideational would mean a “loss of the memory engrams” but motor sequences can be imitated. In ideomotor the posterior areas (e.g. suprmarginal gyrus) are disconnected from the anterior motor control areas - thus the patient cannot pantomime or imitate.

Motor engram damaged Paralyzed hand Ideational Apraxia Ideomotor Apraxia No imitation Motor engram okay Diffuse damage Can imitate Confused motor sequences

ambiguity in defining ideational apraxia, & ideomotor apraxia.
Hécaen and Albert (Hécaen & Albert, 1978) define ideomotor apraxia as a disorder limited to simple, single gestures with preservation of the complex overall idea of the movement. They note the patient often uses a body part to represent the action. They define ideational apraxia as a disruption of the harmonious integration of independent actions into a coherent sequence.
Kenneth Heilman (Heilman, 1973) says that ideomotor apraxia is characterized by an inability to perform movements upon command, a little improvement in imitation, and significance improvement in actual manipulation of the object. He says that ideational apraxia is often defined by improvement in the actual handling of the object. (DeRenzi, Pieczuro, & Vignolo, 1968).
However, in this paper he “redefines” ideational apraxia. He presents three cases with lesions in the dominant parietal lobe. They all had anomic aphasia and were unable to respond at all to movement commands (they would look at their hands, appear perplexed, or make irrelevant movements. However, they performed imitations flawlessly and were able to use actual objects. (Kimura questions the cases??)
Roy and Squire (Roy & Squire, 1994) suggest that differentiating ideomotor from ideational apraxia is largely on the basis of comparing pantomiming and imitation. He states that both are impaired in ideomotor apraxia, whereas only pantomiming is impaired in ideational apraxia.

Dimensions of apraxic testing
Motor Movements
Imitate
meaningless - meaningful
Follow command
meaningless -meaningful
with and without object
Without object: body-as-part, or not
Movement sequences
meaningless-meaningful
with and without objects

Dimensions of apraxic testing: Constructional
Drawing
Imitation
meaningful-meaningless
Memory
Familiar
Unfamiliar
Three-dimensional
Imitation
meaningful-meaningless
Memory
meaningful
Symbolic
Maps
drawing, following

MODELS OF APRAXIA: Roy’s Model
Proposes two systems: conceptual & production
Conceptual: knowledge for gesturing
. knowledge of objects and tools
. knowledge of actions (hammering)
. knowledge of serial order of actions
Production system generates and controls movements
The conceptual system controls the production system in a top-down fashion. (With attention at key choice points)
Roy EA, Squire PA. 1994. Neuropsychology of movement sequencing disorders and apraxia. In Neuropsychology , ed. DW Zaidel, pp. 183-218. New York: Academic Press

Recognition impairments:
e.g. Humphreys: patient could accurately pantomime a gesture with a particular object to a verbal command -- but not to the actual object. Suggests dissociation between object and action. [Why is this not a visual agnosia???]
Ochipa, Rothi, & Heliman: patient could respond to verbal instruction but not imitate gesture displayed by examiner.
A series of studies of gesture recognition. e.g. identify target gesture among set of gestures (video or model)
anterior apraxic subjects could identify correct gesture however presented.
posterior apraxic subjects could not. Heilman argued posterior apraxia = disruption of visuokinetic memory engrams.
Apraxic patients do not recognize body as part pantomimes as incorrect. Since they did recognize spatially incorrect pantomimes as incorrect Roy suggests that these are part of production system but part-as-body are part of conceptual.

Comprehension and apraxia:
Debate between correlation or not between language dysfunction and apraxia and comprehension and apraxia.
What does it mean that the worse apraxia is seen in the worse aphasic patients?

Heilman, Kenneth, Coyle, John M., Gonyea, Edward, & Geshwind, Norman. (1973). Apraxia and agraphia in a left-hander. Brain , 96, 21-28. ---
Previous reports of left-handers losing right hand writing ability without language loss, and of more cases of pure dysgraphia among left-handers.
This case of a left-hander with left hemiplegia who lost right writing ability and has right apraxia. Brain scan & EEG suggest right hemisphere damage, probably middle.
Left-hander - but wrote with right hand
left hemiparesis, slurred speech, but correct grammar & word choice
first confused, then later alert and cooperative.
Stereognosis, two-point - grossly impaired on left
remote memory good, short-term poor
normal language with poor writing spontaneous or to dictation, with improvement for copying. Could spell words out loud, could identify words spelt to him. Typing poor because left keyboard neglected.
No buccofacial apraxia. Apraxia of right arm.
OR, Creative Diagram Making 1010

Paralyzed Apraxic Language OK

Heilman, Kenneth, Coyle, John M., Gonyea, Edward, & Geshwind, Norman. (1973). Apraxia and agraphia in a left-hander. Brain , 96, 21-28.
Cites cases of unilateral apraxia and agraphia with normal language with disconnection of cerebral hemispheres. But these cases were in left hand with inability to name objects in the left hand.
And since the lab tests indicate right middle cerebral, how could this patient have right dominance for language and not be aphasic.
Assumption is that in right-handers writing is controlled by the left hemisphere via the corpus callosum. But it needs both linguistic control and complex motor control. These are usually in the same hemisphere in right-handers and are more frequently housed in different hemispheres in left-handers.

Heilman, M. Kenneth, John Coyle, Edward Gonyea & Norman Geshwind. (1973). Apraxia and agraphia in a left hander. Brain , 96, 21-28.
“ . . .Account for the presence of agraphia in the hand opposite a hemisphere which still serves speech, following a lesion in the hemisphere ipsilateral to that hand.”
Apraxia & agraphia on the right
Case 1: Callosal lesion = right sided agraphia and apraxia
Left hander with Right Dominance for both handedness and speech.
Left hand writing requires no callosal activity
SPEECH Skilled Engrams Motor Control Motor Control

They discuss the Poeck & Kerschensteiner (1971) case
Patient is Right Dominant for both speech and motor skills but writes with the right hand .
So left hemisphere controls right hand via the corpus callosum
Callosal lesion =
apraxic & agraphic with right hand
Left paresis? Damage to callosum at site?
Why not second lesion on left parietal? No other Gerstmann symptoms
SPEECH Skilled Engrams Motor Control Motor Control Paresis

Poeck, K. & Kerschensteiner, M. (1971). Ideomotor apraxia following right-sided cerebral lesion
In which a right sided lesion led to a left agraphia and apraxia, but with aphasia, suggesting a right dominance for language.
Don’t believe that the patient had a left parietal lesion and only part of the Gerstmann syndrome.
This patient was not confused.
Liepmann (1908) proposed that manual dominance is a reflection of one hemisphere’s ability to learn motor tasks more rapidly than the other. Damage to the corpus callosum, or the area where the fibers originate in the dominant hemisphere the patient fails to perform movements with the minor hand. Wyke (1971): patients with left hemisphere lesions do more poorly on bimanual tasks than do those with right hemisphere lesions.
Writing with the left-hand, in right-handers, is under control of the left hemisphere via the corpus callosum.

Poeck, K. & Kerschensteiner, M. (1971). Ideomotor apraxia following right-sided cerebral lesion
So: For some left-handers with right dominance for handedness and right dominance for speech = left hand writing requires no callosal activity. A callosal lesion would produce right-sided agraphia and apraxia.
If the patient is right brained for speech and complex motor skills but writes with the right hand = then the left hemisphere controls the right hand via the corpus callosum. This patient, with a callosal lesion, would be apraxic and agraphic with the right hand but would be able to write with the left hand.
If the patient is left-brained for speech and right-brained for motor skills and writes with the right hand = then the writing requires crossing the corpus callosum twice. He must relay linguistic information from left to right to arouse the appropriate motor sequence. Then he must relay the motor sequence back to the left hemisphere which controls the right hand. A callosal lesion in this patient = right apraxic and agraphic (disconnection of motor-dominant hemisphere), agraphic in left hand because of disconnection from speech-dominant hemisphere. Apraxic to verbal commands in the left hand, with preservation of object handling and imitation.
In pathological left-handers the shift may not be complete, complicated the possible scenarios.
Notes that Hecaen and Sauguet (1971) found apraxia occasionally after left-sided lesions and none after right-sided. But in cases such as this one the left-hander improves (improvement in apraxia) over time: left handers may show more improvement in apraxia, (also for aphasia).

BACK TO THIS CASE:
Patient is left dominant for speech and right dominant for motor skills and writes with the right hand.
Then writing requires crossing the corpus callosum twice.
Must relay linguistic information from left to arouse the appropriate motor right to sequence.
Must relay the motor sequence back to left hemisphere which controls right hand.
Right hemisphere lesion destroying R motor engrams
SPEECH Skilled Engrams Motor Control Paresis Motor Control

Heilman, Kenneth, Gonyea, Edward, & Geshwind, Norman. (1974). Apraxia and Agraphia in a right-hander. Cortex, 10(3), 284-288.
Usually agraphia is reported with left hemisphere aphasia or Gerstmann’s syndrome. This is a case of a right-handed man with agraphia and apraxia - but not aphasia.
Right hemiparesis, right homonymous hemianopsia, right-sided facial weakness. Neglect of visual, auditory, somesthetic stimuli to RIGHT side of space. Depressed with frequent crying spells.
Reading = neglect of right side of space, could read sentence if moved to left visual field.
Spontaneous writing bad, writing to dictation not much better, copying poor, better on the left.
Movements, such as show how you use a key, were accompanied by adequate verbal description (“You put it into the lock, turn it a quarter-turn to the left, and open the door.”) but he raised his fist in the air and performed poor representations of these movements.
Poor left middle cerebral artery perfusion and left internal carotid occlusion.

Heilman, Kenneth, Gonyea, Edward, & Geshwind, Norman. (1974). Apraxia and Agraphia in a right-hander. Cortex, 10(3), 284-288.
Notes previous cases (Liepmann and Maas, 1907; Geshwind & Kaplan, 1962) of unilateral left apraxia and agraphia without aphasia with damage to midline corpus callosum. They also show poor naming of objects held with the left hand.
Notes Ajuriaguerra & Heacaen (1960) described patients who wrote on only one side of page and failed to form straight lines = called them spatial dysgraphics. But they could produce – this patient is less able to write than reflected in a spatial dysfunction.
Chedru & Geshwind (1972). Described agraphics with little language disorder, but confusional states.
This patient was not confused. Other components of Gerstmann’s syndrome not present.
Previous case (Heilman, 1973) reported a left-handed patient with left hemiplegia, agraphia and apraxia in right hand, and no aphasia. They concluded left hemisphere speech and right hemisphere dominance for handedness,…crossed aphasia in left-handers.
In this case they argue for dominance for engrams for complex motor acts in the left hemisphere and speech dominance in the right hemisphere.

SPEECH Skilled Engrams Right-Sided Neglect Heilman, Kenneth, Gonyea, Edward, & Geshwind, Norman. (1974). Apraxia and Agraphia in a right-hander. Cortex, 10(3), 284-288. ?

Anatomical Considerations in the Motor Apraxias
Gazzaniga, Bogen and Sperry (1967) found a wide variation in apraxic symptoms in nine patients with division of the cerebral commissures. However, they found that the hemispheres were able to exert voluntary motor control over both the homolateral and contralateral limbs. They suggest that the variations in reports of dyspraxia following callosal lesions may be due to differences in extracommissural damage, diaschisis, and so on. This is not a new claim. Kurt Goldstein had earlier objected to the “disconnectionist” models of apraxia and proposed that less localized disturbances accounted for the disorder.

Kertesz, A. and J. Ferro (1984). “Lesion size and location in ideomotor apraxia.” Brain 107 : 921-933.
used CT scans to assess lesion size and location and the severity of apraxia in 177 acute and chronic right-handed left-hemisphere stroke patients.
positive correlation between overall severity of apraxia and the size of the lesion.
In eight of nine cases of severe apraxia with small lesions the damage were primarily subcortical in the frontal lobes. None of the lesions extended to the basal ganglia. Generally they were located in the white matter near the lateral ventricles (periventricular white matter). These patients also had severe nonfluent aphasia.
A single case had damage in the left inferior temporo-occipital and splenial region causing moderate Wernicke’s aphasia, alexia with agraphia, and bilateral ideomotor apraxia. They note this is an unusual finding since neither damage to the splenium nor damage this far posterior are associated with apraxia. They suggest that the CT scan may not have picked up more extensive areas of damage.
Nine acute patients and 14 chronic patients had large left hemisphere lesions without apraxia . Generally these patients had large frontocentral cortico-subcortical lesions and some also had inferior parietal lobe lesions. Eight out of 16 of these patients had larger left frontal lobes and larger right occipital lobes which is the reverse of the typical pattern of asymmetry seen in right-handers.
Thus damage to the periventricular white matter, which could disrupt fronto-parietal connections and the occipital-frontal fasciculus, and the superior longitudinal fasciculus (which Geschwind, 1965, implicated in performing movements to verbal command). However, the superior longitudinal fasciculus was spared in some of the patients.

Kertesz, A. and J. Ferro (1984). “Lesion size and location in ideomotor apraxia.” Brain 107 : 921-933.
Disrupting the parietal and frontal areas corresponds to theories proposed by both Liepmann and Geschwind; namely, it interrupts the visuo-kinesthetic patterns from reaching the motor programming areas of the frontal lobes. They propose that small lesions can disrupt the integration of information from a number of these critical pathways when they occur near the anterior fronto-parietal area subcortically. Alternatively, more posterior lesions would have to cover a wider area in order to create the same disturbance.
They noted, however, that in some cases large left hemisphere lesions including the parietal lobe and/or the fronto-parietal connections failed to produce apraxia. They suggest that bihemispheric representation of function is a probable explanation for these cases. The observation that fifty-percent of these patients had unusual asymmetry in frontal and occipital lobe size supports this possibility. Though they caution that this asymmetry was also observed in two of the apraxic patients with small lesions.

Disorders Of Skilled Movement Not Caused By Weakness

by Nirmala last on Oct 23, 2008

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