1.  What are some of the most common speech characteristics of hypokinetic dysarthria?
  reduced vocal loudness, harsh or breathy vocal quality and abnormal speaking rates (slow speaking rates but rushes of fast speech)

2.  In what way is hypokinetic dysarthria unique in comparison to other dysarthrias?
 a.  Only dysarthria in which increased rate of speech may be one of the symptoms
 b.  It is the only one in which the vast majority of the cases share the same etiological factor (Parkinsonism)

3.  What parkinsonian symptoms have the greatest effect on speech?  Muscle rigidity, reduced range of motion and slowed movement.

4.  Where is the cite of lesion for hypokinetic dysarthria?  Basal ganglia or damage to the basal ganglia’s neural connections to other parts of the  CNS

5.  What does hypokinetic mean and give examples of how it is expressed?
 Hypokinetic means less motion describing decreased range and frequency of movement.
 Expressed in the festinating gait (baby step type of walking) and the masked facies.

6. List and define some of the collection of symptoms of parkinsonism.
 a.  tremor:  most commonly in fingers and hands; resting tremors
 b.  bradykinesia:  slow, labored, reduced range of movements (shuffling walk and masked facies are examples) [not caused by muscle weakness but to dysfunction in the basal ganglia.
 c.  Muscle rigidity: result of increased muscle tone; there will be a constant resistance to the movement. In some instances, there are intermittent changes in rigidity described as “cogwheel resistance”.  Difference between spasticity and rigidity are in spasticity there is resistance up to a point then a relaxation of the muscle.  In rigidity the resistance is constant
 d.  Akinesa: a delay in the initiation of movement; may appear to get stuck in a motion and unable to continue until someone touches them; may be unable to stop a motion once initiated; in speech there is a delay in response to questions
 e.  Disturbances of postural reflexes: caused by basal ganglia dysfunction: the basal ganglia is not helping to regulate postural reflexes through neural connections with the extrapyramidal system.
 -difficulty maintaining balance while walking
 -normal swing is absent; arms are held stiffly at the side
 -may fall if pushed because they are unable to quickly shift their center of balance
 -may not be able to get out of a chair
 f.  other
 - depression
 -swallowing
 -dementia
 -dysarthria.

7. Define:
Basal ganglia: a collection of subcortical, gray matter that plays a role in controlling movement; consisting of the caudate nucleus, globus palidus, and putamen
Striatum: the caudate nucleus and the putamen.
Dopamine: an inhibitory neurotransmitter that tends to slow neural activity within the striatum, produced by neurons in the substantia nigra (gray matter located near the basal ganglia)
Acetylcholine: affects the function of the basal ganglia; has an excitatory effect on these areas of the brain and facilitates neural firing.

8.  Describe the neural control circuit that connects the basal ganglia to the cortex.
Neural fibers descend from the cortex transmitting information about planned upcoming movements .  The BG smoothes and refines the movements especially those that are slow and continuous.  The BG sends up the refined neural impulses for planned movements up through the thalamus up to the motor cortex, where they are transmitted through the pyramidal system to the lower motor neurons and out to the muscles.

9. What is parkinsonism caused by? A reduction of dopamine in the striatum causing too much excitatory neurons acting on the neurons compared to the amount of inhibitory neurotransmitters resulting in rigidity and bradykinesia

10. What are some of the known causes of reduced dopamine in the striatum?
 Drugs, toxic poisoning, infections, tumors, head injury, anoxia, CVA

11.  What is the pharmacological treatment?
L-dopa is converted to dopamine by the brain
Anticholinergic drugs to decrease effects of acetycholine
Combination of L-dopa and Anticholinergic drugs

12.  What are the side effects of the drugs?
L-dopa: gastrointestinal disturbance, blood pressure, insomnia, agitation, and psychiatric symptoms, and abnormal involuntary movments.
Anticholinergic: dry mouth, dizziness, clumsiness, dialated pupils, emotional outbursts, confusion, psychiatric
The drugs eventually become ineffective

13.  Define the etiologies of Hypokinetic dysarthria.
Idiopathic Parkinson’s Disease: Most common form of parkinsonism and single most frequent cause of hypokinetic dysarthria; The disease is the result of the progressive degeneration of dopamine producing neurons in the substantia nigra.
Neuroleptic – Induced Parkinsonism: caused by neuroleptic drugs used in treating psychotic patients. Effects usually occur within 2-4 weeks of taking the drug. Some of the drugs increase the amount of acetylcholine in the basal ganglia.  Patients have to take other drugs to treat the parkinsonian symptoms: L-dopa cannot be used because it increases psychotic symptoms.
Postencephalitic Parkinsonism: caused by viral encephalitis. Effects occur several weeks or months after acute stage of the infection. Cognitive effects are associated with children who develop postencephalitic parkinsonism: increased distractibility, impaired abstract reasoning.  TX: L-dopa
TBI: Repeated blows (boxing: punch drunk encephalopathy) characterized by memory deficits, slowed movements, and dysarthria.
Cerebral anoxia: selectively affects basal ganglia; bradykinesia and rigidity may appear days or weeks after; Cognitive and pyramidal system deficits will be present as well.
Toxic Metal Poisoning: Exposure to manganese used in manufacturing iron, aluminum and copper alloys occurs in miners.  Effects: irritability insomnia and emotional outbursts; dementia, and parkinsonian signs
Stroke:  Single stroke: parkinsonian symptoms on the side of the body opposite to the lesion with majority of cases showing spontaneous recovery; Multiple strokes: numerous associated disorders including speech and language problems.

14. Generally what are the most defining speech characteristics of hypokinetic dysarthria?
Placement of the articulatory movements appear accurate but the range of the movements is restricted;
Speech movements appear compressed and abbreviated.
Speech difficulty is caused by bradykinesia (reduced range and speed of movement), akinesia (delays in the initiation of movement) and muscle rigidity.  Tremor may also be present.

15. Define the characteristics of the processes of speech for hyopokinetic dysarthria.
 a.  Prosody:
  -monopitch, reduced stress and monoloudness most prominent speech characteristics.
  -inapproprite silences: due to akinesia
  -speech rate abnormalities:
   increased rate: related to inability to stop a voluntary motion causing        blurring of articulation;
   short rushes of speech: a stop-and-go quality with a brief pause         followed by quick production of several words;
   decreased rate
 b.  Articulation:
  -imprecise consonants caused by reduced range of movements of articulators
  -repeated phonemes usually at the beginning of an utterance or after a pause
  -palilalia: compulsive, increasingly rapid repetition of a word or phrase with the utterance fading into    a soft blurred mumble (most evident when responding with a single word utterance)
   may be related to the inability to stop a voluntary movement once started.
 c.  Phonation:
  -harsh or breathy voice quality caused by incomplete vocal fold adduction (air leaking through a partly    open glottis causes turbulent noise
  -pitch differences may vary
 d.  Respiration: may have breathing rates faster than normal; may have paradoxical movements of diaphragm  and the chest muscles. Reduced range of movement in respiratory muscles result in shallow breath support,  poorly controlled exhalations and short breathing cycles (may be a cause for short rushes of speech and soft  phonation
 e.  Resonance: if present, mild

What are key evaluation tasks for hypokinetic dysarthria?
 a.  Conversational speech
  -monopitch, reduced stress, monoloudness, inappropriate silences, short rushes of speech
 b. AMR’s articulation errors –imprecise articulation, variable rates and blurring
 c.  Vowel prolongation to assess for harshness and  breathiness
 d. The above can also be used to assess decreased loudness, pitch and repeated phonemes

What is the TX for hypokinetic dysarthria?
Drugs: L-dopa and anticholinergic drugs
Lee Silverman Program an increased loudness program; improves rate, vf adduction, loudness, articulation precision
Articulation:
rate reduction: to allow articulators more time to reach the targets and to accurately produce phonemes; prosody may also appear more natural
  pacing boards
 Others are limited: hand/finger tapping (cant maintain a steady rate), alphabet boards (cognitive and  conspicuous, DAF (may work if it does there are nice options here—in the ear DAF); metronomes (carryover  not good)
Stretching: to reduce tonicity:  this would be a very short term temporary fix.
Articulation TX: intelligibility drills, exaggerated consonants, minimal contrast drills
  (phonetic placement—most people cant think about tongue placement while they are talking)

Phonation:
 Pushing and pulling for vf adduction (carry over)
 *Head turning and pressure for vf adduction (can be done while speaking)
 Hard glottal attack (carry over)
 *Voice amplifiers
 Instrumental biofeedback: Visi-Pitch for pitch and loudness feedback (carryover problems)
Respiration:
 Shallow breath support may cause shortened phrases and decreased loudness and breathiness;
a.  speak immediately on exhalation
b.  cues to inhale completely
c.  stop phonation early
d.  optimal breath group

Prosody:
a.  intonation profiles (lines that define pitch cues)
b.  contrastive stress drills
c.  Chunking utterances (phrasing lines cues to inhale)