Lecture 19 - Motor Systems 2

Question 1

Cause of Motor Disorders

Answer 1

• Pathological changes of certain areas of the brain are the main causes of most motor disorders. (brain injury/stroke/
• Or with subcortical, there may be neurogenesis/neural decline issues
• The way humans move requires many parts of the brain to work together to perform a complex process.
• Some conditions arise from cortical damage.
• Others arise from selective damage to subcortical structures.

Question 2

Cortical Sensorimotor Disorders

Answer 2

Cortical disorders that are primarily somatosensory in nature:

• Apraxia
• Phantom sensation

Question 3

What is Apraxia

Answer 3

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex) in which the individual has difficulty with the motor planning to perform tasks or movements when asked

• A deficit in performing skilled voluntary movements that is not attributable to primary sensory problems, primary motor problems, paralysis or muscle weakness.
• Actions become unorganized or inappropriate.

Question 4

Types of Apraxia (8)

Answer 4

• Ideomotor apraxia – a person cannot perform simple gestures/movements in response to a command. Not able to put together HOW not what, they understand what they need to do…
• Ideational apraxia – inability to correctly sequence a series of movements.
• Callosal apraxia – Left-hand apraxia following damage to the corpus callosum. Characterized by both ideational and ideomotor symptoms.
• Constructional apraxia – the inability to construct a complex object using visuospatial information.
• Oral apraxia – inability to conduct skilled movements of the face following a command. (can’t smile on command. Meaningful and non-meaningful both affected?)
• Limb apraxia – impairment in fine or precise movements of the limbs. (can’t stir tea, etc. Often cannot mimick…use finger to stir tea)
• Dressing apraxia – deficit in dressing oneself. Problems both with orientating limbs and manipulating clothes.
• Gaze apraxia – people can move their eyes in any direction but cannot shift their gaze intentionally.
• Alien limb – more about inhibition issues

Question 5

Brain Regions: Apraxia

Answer 5

• Usually due to a lesion located in the dominant (usually left) hemisphere of the brain, typically in the frontal and parietal lobes. (this is why it’s generally the one hand
• Lesions may be due to stroke, acquired brain injuries, or neurodegenerative diseases such as Alzheimer’s disease or other dementias, Parkinson’s disease, or Huntington’s disease.
• Ideomotor apraxia: typically due to a decrease in blood flow to the dominant hemisphere of the brain and particularly the parietal and premotor areas.
• Ideational apraxia: associated with lesions in the dominant hemisphere near areas associated with aphasia.
• Constructional apraxia: often caused by lesions of the inferior non-dominant parietal lobe.

Question 6

Treatment: Apraxia

Answer 6

•Not well developed. Can include speech therapy, occupational therapy, and physical therapy. More about managing symptoms.

Gesture therapy:

•The patient is instructed to make gestures (either using objects or symbolically meaningful and non-meaningful gestures) with progressively less cuing from the therapist.

Question 7

Case study Jimmy - phantom limb

Answer 7

felt that his phantom hand was always agonizingly clenched, with his phantom fingernails digging into his missing hand.

• A mirror was put between Jimmy’s arms and asked him to move both his phantom and healthy limb simultaneously while looking at the reflection of the healthy limb.
• This fooled Jimmy’s brain into thinking his phantom was moving in a normal way.
• Creating a sensory conflict
• Jimmy felt his clenched fist release almost immediately.

•

Question 8

Mirror Neurons

Answer 8

• A mirror neuron is a neuron that fires both when a human acts and when the human observes the same action performed by another.
• Thus, the neuron “mirrors” the behaviour of the other, as though the observer were itself acting.
• Knowledge of mirror neurons applied to phantom limb syndrome: mirror neurons firing when an individual watches someone moving a limb suggests that visual perception might play an important role in creating the sensation of movement.

Question 9

MVF Therapy

Answer 9

Mirror Visual Feedback therapy

Question 10

Subcortical Sensorimotor Disorders

Answer 10

• Subcortical such as basal ganglia,
• Parkinson’s Disease
• Huntington’s Chorea
• These^twosimilar
• Tardive Dyskinesia
• Tourette Syndrome

Question 11

Parkinson’s Disease - 4 major symptoms

Answer 11

Four major symptoms:

• Tremor at rest (body movement when not wanted/initiated)
• Akinesia (slowness in whole body movement such as getting out of a chair, when walking-can’t initiate arm swing)
• Rigidity (looks like slowness, but muscles are stiff)
• Disturbance in posture (often seen as a shuffle-walk)

Question 12

How does Parkinsons work?

Answer 12

• Genetic etiology. Been linked to enviro interaction too (pesticides, syphilis, etc)
• Neural degeneration occurs along the striatal dopamine pathways which extend from the substantia nigra to the components of the basal ganglia.
• Substantia nigra degenerates selectively.

Question 13

Treatment of Parkinson’s

Answer 13

•Medication:

• Treated with i-dopa.
• I-dopa targets and reduces symptoms dramatically initially, although its effectiveness decreases over time, generally have to up dosages over time
• May be on anxiety meds as well depending on the case

Surgery:

• Thalamotomy - 80% effective. (lesion of the thalamus) usually when unilateral issues?
• Pallidotomy –80% effective in reducing akinesia.(lesioning the globus palladus)

•

Question 14

Huntington’s Chorea (or Huntington’s disease)

Symptoms

Answer 14

Symptoms:

• Dancelike, writhing movements (Hence name Chorea)
• Intellectual deterioration, often into dementia
• Eventual impairment of purposeful movement.
• Changes in personality, memory, and processing speed.
• Late age of onset, 30-50 years old.. Important, and to know that it is highly heritable (people pass it on before they know they have it…) (aren’t there issues evolutionarily?)

Question 15

Huntington’s Chorea

Answer 15

How does it work?

• Highly genetic/heritable – HD gene mapped to chromosome 4 (50% if you have a parent with HD).
• Mutation is called a nucleotide triplet repeat, and the DNA affected codes for the protein huntingtin. Too many copies of a sequence result in HC.
• Woody Guthrie (died of Huntingtons. People though schizophrenia, alcoholism, but yeah)

Question 16

Brain Regions for Huntingtons

Answer 16

What goes on in the brain?

• Most prominent effects involve damage to the striatum (both the caudate nucleus and the putamen). (these are parts of the basal ganglia). Issues of inhibition. When basal ganglia degenerates (reduced volume due to neural degeneration), we see both over and under inhibition.
• Other areas affected include the substantia nigra, layers 3, 5 and 6 of the cerebral cortex, the hippocampus, the cerebellum, parts of the hypothalamus and parts of the thalamus.
• These areas are affected according to their structure and the types of neurons they contain, reducing in size as they lose cells.

Question 17

Huntington’s Chorea medication

Answer 17

Medication:

• The best evidence for treatment of the movement problems is with tetrabenazine.
• Hypokinesia and rigidity early on can be treated with antiparkinsonian drugs, myoclonic hyperkinesia can be treated with valproic acid.
• SSRIs and mirtazapine have been recommended for depression, while atypical antipsychotic drugs are recommended for psychosis and behavioral problems (same as anyone else without the disease)

Question 18

Huntington’s Chorea Treatment

Answer 18

Multidisciplinary care:

• Physical therapy, occupational therapy, and speech therapy.
• Weight loss and eating difficulty management. (often risks of choking/can’t swallow, therefore weight loss)
• Full-time care is required in the later stages of the disease.

Question 19

Tardive Dyskinesia

Answer 19

• Affects approximately 30% of long term users of anti-psychotic medication.
• Movements are increased rather than decreased because dopaminergic neurons in substantia nigra are chronically under-stimulated when someone takes antidopaminergic medication for long periods of time.
• These neurons then become super sensitive to stimulation and when receptors are stimulated the result is unwanted movement.

Question 20

Tardive Dyskinesia signs

Answer 20

• Grimacing
• Tongue movements
• Lip smacking
• Lip puckering
• Pursing of the lips
• Excessive eye blinking

•

Question 21

Treatment of dyskinesia

Answer 21

Prevention:

•Achieved by using the lowest effective dose of a neuroleptic for the shortest time.

Medication:

• Valbenazine was approved by the FDA for tardive dyskinesia in April 2017.
• Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia.
• Vitamin B6 has been reported in two studies to be an effective treatment for TD.
• Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia.

Question 22

DSM-5 Motor Disorders

Answer 22

Motor disorders are defined in the DSM-5 as a new sub-category of neurodevelopmental disorders.

Include:

• Developmental coordination disorder.
• Stereotypic movement disorder.
• Tic disorders including Tourette syndrome.

Question 23

Tourette Syndrome

Answer 23

Symptoms:

• Motor tics (head jerking, blinking, shrugging, grimacing, spastic movements of hands and arms).
• Only 10% of people with this swear
• Vocal tics (palilalia; repeating words, echolalia; compulsive repeating of words spoken by others, coprolalia; uttering of obscenities.
• Tics tend to increase in complexity.
• Symptoms usually emerge early in life.
• Trying to suppress does not work, usually gets worse
• Spectrum disorder mild-severe. Most adults have less-severe/can cope better

Question 24

DSM-5 Diagnosis Tourettes

Answer 24

DSM-5:

•Tourette’s may be diagnosed when a person exhibits both multiple motor and one or more vocal tics over the period of a year; the motor and vocal tics need not be concurrent.

•

•The onset must have occurred before the age of 18, and cannot be attributed to the effects of another condition or substance (such as cocaine).

Question 25

Prevalence tourettes

Answer 25

• Seems to be a genetic component, over 1/3 of people with Tourette’s also have an afflicted family member.
• Three times more prevalent in males.
• Some studies have linked it to a gene on chromosome 18.

Question 26

Tourette Syndrome brain

Answer 26

•Tics are believed to result from dysfunction in cortical and subcortical regions, the thalamus, basal ganglia and frontal cortex (inhibition).

•

• Neuroanatomic models implicate failures in circuits connecting the brain’s cortex and subcortex, and imaging techniques implicate the basal ganglia and frontal cortex.(and communication between them) (but not seen in females?)
• People with the syndrome tend to have reduced basal ganglia volume.
• Dysfunction in dopamine, serotonin, and norepinephrine

Question 27

Treatment: Tourette Syndrome

Answer 27

• Medication is reserved for more severe symptoms which interfere with functioning.
• Treated with drugs that reduce dopamine and to a lesser extent norepinephrine transmission.
• Often comorbid with ADHD and OCD though not the cause, more so the symptoms trying to manage
• Some new drugs that target GAPA agonists have also been used to treat it.

Question 28

Treatment: Tourette Syndrome

Answer 28

Behavioral:

•Relaxation techniques.

Psychological:

•Therapies to cope psychologically

Question 29

Strength-Based Assessment

Strengths-based apporach

Answer 29

What is it?

• Therapeutic conversation that focuses on drawing out assets, competencies, favourable conditions, and potential of the person. (what’s important to the client, what doe YOU want to work on? That which is in the client’s control, strengths to build on)
• Supports the person by focusing on what works well and the dreams and goals they want to achieve (client-centered).
• Building on a person’s existing abilities.
• Focusing on what the person can do rather than on what they cannot do.
• Attending to how the person can manage their difficulties using what is within their control.