Cortex Flashcards

1
Q

Spastic (UMN) dysarthria

A

3 main cuases: ALS, progressive supranuclear palsy, pseudobulbar state secondary to chronic ischaemic disease in the subcortical white matter.

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2
Q

Flaccid (LMN) dysarthria

A

causes are generalised motor neuron disorders, myasthenia gravis. CNVIII involvememtn causes greatest difficulties producing labial sounds as ‘puh’

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3
Q

Hypoglossal nerve lesions produce difficulties with sounds…?

A

with lingual sounds such as #tuh#.

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4
Q

Scanning (cerebellar) dysarthria

A

halting speech, uncoordinated pattern, awkward volume modulations and separations between words. Most common cause is advanced multiple sclerosis.

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5
Q

Oral phase dysphagia:

A

hypoglossal nerve lesions. When the tongue is sitcked out, deviations to a side suggest either ipsilateral hypoglossal nuclear or nerve lesion or contralateral hemispheric lesion.

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6
Q

Pharyngeal phase dysphagia

A

supranuclear lesions. Because the motor neurons of nucleus ambiguous receive supranuclear inputs from both hemispheres, unilateral lesions do not produce dysphagia. Bilateral lesions are quite common in patients with the pseudobulbar state characterised by dysphagia, spastic dysarthria and emotional incontinence.

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7
Q

LOWER BRAINSTEM (BULBAR) SYMPTOMS

A

unifying feature of facial movement, speech, swallowing – the lower motor neurons that control them lie within the pons and medulla. They occupy a small volume → a tiny focus of infarction, inflammation or neoplasia leads to simulataneous facial weakness , dysarthria and dysphagia.

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8
Q

Facial weakness: DDx

A

stroke or Bells palsy (ie central vs peripheral)

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9
Q

• Cortical lesions in facial weakness. features

A

do not tend to affect the upper half of the face as motor neurons receive scan cortical input there. Pontine stroke can produce facial weakness that appears peripheral in origin.
• Hand weakness ipsilateral to facial weakness suggests cortical pathology

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10
Q

• Combination of facial weakness and dysphagia point to a lesion …

A

involving both medulla and pons

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11
Q

• Paralysis of ipsilateral conjugate gaze or ipsilateral eye abduction suggests a lesion in

A

a lesion in the pons (facial nerve fascicles cross the abducens nucleus and nerve). Contralateral limb weakness due to a lesion of the adjacent corticospinal tract often present

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12
Q

• Isolated facial weakness in both upper and lower halves points to a lesion

A

to a lesion of CNVII in the facial canal distal to the takeoof of the chorda tympani.

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13
Q

Dysarthria is

A

a speech disorder in which the mechanism for speech is damaged by lesions in the corticobulbar pathways; in one or more CN nuclei or nerves V, VII, IX, X, and XII; in the cerebellum; or in the muscles that produce speech sounds. Dysarthria - by dysfunction of the phonation, articulation, resonance, or respiration aspects of speech.

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14
Q

what features of language depend on Broca’s area

where is it located

A

The ability to think of the right words, to program and coordinate the sequence of muscle contractions necessary to produce intelligible sounds, and to assemble words into meaningful sentences depends on Broca’s area (areas 44 and 45) within the inferior frontal gyrus, located just anterior to the motor cortex controlling the lips and tongue.

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15
Q

what depends on the wernickes area and where is

A

The ability to comprehend language, including speech, is dependent on Wernicke’s area. Located in the posterior part of the superior temporal gyrus within the auditory association cortex (area 22).

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16
Q

what does the The arcuate fasciculus do?

A

The arcuate fasciculus provides an association pathway within the hemisphere white matter, connecting Wernicke’s and Broca’s areas. Arcuate fasciculus connects the speech comprehension area (Wernicke’s area) with the area responsible for production of speech (Broca’s area), damage to this white matter tract → impairment of repetition.