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Vocabulary flashcards summarizing key terms, syndromes, anatomical sites, and etiologies related to neurogenic mutism and motor-speech disorders.
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Mutism
Complete absence of speech; may be deliberate, psychiatric, or neurogenic in origin.
Neurogenic Mutism
Speech absence caused by neurological impairment (e.g., dysarthria, AOS, aphasia, cognitive-affective conditions).
Anarthria
Speechlessness from extreme neuromuscular loss—end-stage, severe dysarthria with intact language/cognition.
Dysarthria
Motor-speech disorder from neurological damage affecting muscular control of speech mechanisms.
Flaccid Dysarthria
Dysarthria due to LMN damage; hypotonia and weakness—rarely results in anarthria unless multiple cranial nerves bilaterally impaired.
Spastic Dysarthria
Dysarthria from bilateral UMN damage; strain-strangled voice, slow effortful speech—common cause of anarthria.
Hypokinetic Dysarthria
Basal ganglia disorder (e.g., Parkinson’s); reduced loudness, rapid rate, monopitch—can progress to anarthria.
Ataxic Dysarthria
Cerebellar disorder; irregular articulatory breakdowns, scanning speech—seldom leads to mutism.
Hyperkinetic Dysarthria
Basal ganglia control circuit pathology; involuntary movements—rarely causes mutism.
Mixed Dysarthria
Combination of two or more dysarthria types; most frequent pathway to anarthria in neurodegenerative disease.
Locked-In Syndrome (LIS)
Anarthria plus quadriplegia with eye-blink/vertical gaze preserved; cognition intact, communication via eyes.
Quadriplegia
Paralysis of all four limbs; characteristic of LIS.
Brainstem Stroke
Common etiology for LIS with high early mortality and limited recovery.
Biopercular Syndrome
Foix-Chavany-Marie syndrome; bilateral opercular lesions causing severe voluntary orofacial paralysis and mutism with preserved reflexive/emotional movements.
Rolandic (Anterior) Operculum
Lower pre- and postcentral gyri region; bilateral damage causes biopercular syndrome.
Cerebellar Mutism
Transient postoperative mutism (mainly children) after posterior fossa surgery; often evolves to ataxic dysarthria.
Posterior Fossa
Cranial cavity region housing cerebellum & brainstem; surgical lesions here may trigger cerebellar mutism.
Diaschesis
Loss of function in intact brain areas connected to damaged regions; proposed mechanism for cerebellar mutism.
Traumatic Midbrain Anarthria
Mute period post-trauma with severe articulatory immobility, later mixed spastic-hypokinetic dysarthria.
Apraxia of Speech (AOS)
Motor-programming disorder causing impaired speech sequencing; initial mutism possible post-stroke.
Nonverbal Oral Apraxia (NVOA)
Inability to perform purposeful, non-speech oral movements; commonly accompanies AOS and mutism.
Akinetic Mutism
Extreme abulia from mesial frontal/SMA lesions; alert but profoundly apathetic and mute.
Abulia
Diminished motivation and initiative; milder form of akinetic mutism.
Supplementary Motor Area (SMA)
Medial frontal cortex zone; lesions contribute to akinetic mutism and speech initiation deficits.
Reticular Activating System (RAS)
Brainstem network governing arousal; damage may yield akinetic mutism‐like states.
Coma
State of unresponsiveness from widespread cerebral or brainstem injury.
Vegetative State
Wakeful unawareness following coma; preserved brainstem functions but no purposeful responses.
Minimally Conscious State
Condition of limited but definite awareness—visual tracking, simple command following, occasional words.
Neurogenic Stuttering
Acquired dysfluency linked to multifocal CNS lesions; differs from developmental stuttering.
Palilalia
Pathological reiteration of one’s own speech; associated with basal ganglia/frontal damage.
Echolalia
Automatic repetition of others’ speech; seen in diffuse or left-hemisphere lesions, dementia, etc.
Attenuated Speech / Hypophonia
Marked reduction in voice loudness often tied to hypokinetic dysarthria or limbic/thalamic pathology.
Disinhibited Vocalization
Involuntary outbursts (e.g., coprolalia) due to diffuse or basal ganglia lesions; seen in Tourette’s.
Right Hemisphere Aprosodia
Impaired production/interpretation of prosodic cues for emotion or emphasis; often after RH stroke.
Functional Speech Disorder (FSD)
Speech change of psychogenic origin; inconsistent with neurogenic patterns and often improves rapidly with suggestion.
Primary / Secondary Gain
Psychological benefits (internal or external) that may reinforce functional symptoms.
Corpus Callosotomy
Surgical severing of corpus callosum for seizure control; may cause transient mutism with spared comprehension.
Ictal Speech Arrest
Transient mutism during partial seizures; resolves post-ictally.
Myasthenia Gravis
Autoimmune neuromuscular disorder; generalized weakness—bilateral cranial nerve involvement can cause flaccid anarthria.
Guillain-Barré Syndrome
Acute demyelinating polyneuropathy; widespread LMN weakness potentially leading to flaccid mutism.
Wilson’s Disease
Genetic copper-metabolism disorder; basal ganglia damage may produce mixed dysarthria progressing to anarthria.
Torus Palatinus (Tori Palatini)
Benign bony growth on hard palate; usually asymptomatic, unrelated to neurogenic speech disorders.