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Tremor by Mind Map: Tremor

1. 6. Management

1.1. include

1.1.1. Levodopa

1.1.1.1. able to cross BBB (unlike dopamine)

1.1.1.2. contraindicated with

1.1.1.2.1. Vitamin B6

1.1.1.2.2. MAO inhibitors

1.1.1.3. given with

1.1.1.3.1. DOPA decarboxylase inhibitors

1.1.2. MAO-B inhibitor

1.1.2.1. like

1.1.2.1.1. Selegiline

1.1.2.1.2. Rasagiline

1.1.2.2. inhibits dopamine breakdown

1.1.3. COMT inhibitor

1.1.3.1. like

1.1.3.1.1. Entacapone

1.1.3.1.2. Tolcapone

1.1.3.2. inhibits L-DOPA/ Dopamine breakdown

1.1.4. Dopamine agonist

1.1.4.1. like

1.1.4.1.1. Bromocriptine

1.1.4.1.2. Apomorphine

1.1.4.1.3. Pramipexole

1.1.4.1.4. Ropinirole

1.1.5. Dopamine reuptake inhibitor

1.1.5.1. like

1.1.5.1.1. Amantadine

1.1.6. Anticholinergics

1.1.6.1. like

1.1.6.1.1. Benztropine

1.1.6.1.2. Trihexphenidyl

1.1.6.1.3. corrects imbalance between ACh and Dopamine

2. 2. Physiology

2.1. Basal Nuclei

2.1.1. Modifies Motor Output

2.1.2. Input

2.1.2.1. Cerebral Cortex

2.1.2.2. Substansia Nigra

2.1.2.3. Thalamus

2.1.2.4. Raphe Nucleus

2.1.3. Output

2.1.3.1. Thalamic Nuclei

2.1.3.2. Reticular Formation

2.1.3.3. Substansia Nigra

2.1.4. Pathways

2.1.4.1. Direct

2.1.4.1.1. Stimulates Motor Activity

2.1.4.2. Indirect

2.1.4.2.1. Inhibits Motor Activity

2.2. Cerebellum

2.2.1. Maintains

2.2.1.1. Balance

2.2.1.2. Muscle Tone

2.2.1.3. Posture

2.2.2. Coordinates

2.2.2.1. Muscle Movement

2.2.3. Input

2.2.3.1. Dorsal Spinocerebellar Tract

2.2.3.1.1. Information From Muscle Spindles

2.2.3.2. Ventral Spinocerebellar Tract

2.2.3.2.1. Information from Golgi Tendon Organs

2.2.3.3. Cuneocerebellar Tract

2.2.3.3.1. Information From Head, Neck & Upper Limb

2.2.4. Output

2.2.4.1. Limb Movement Control

2.2.4.1.1. Thalamic VL nuclei

2.2.4.2. Trunk Movement Control

2.2.4.2.1. Vestibular Nuclei

2.2.4.2.2. Red Nuclei

2.2.4.2.3. Reticular Formation

2.3. Ions and Contraction

2.3.1. Depends on

2.3.1.1. Muscle Type

2.3.2. Main Ion

2.3.2.1. Calcium

2.3.3. Mechanism

2.3.3.1. Power Stroke & Cross-Bridge Cycling

3. Neurodegeneration of substantia nigra

3.1. ↑ Inhibitory signals to cortex

3.2. ↓ stimulatory signals to the cortex

4. 3. Movement Disorders

4.1. result from

4.1.1. damage to basal ganglia

4.2. Types

4.2.1. Parkinosn's

4.2.1.1. Most common

4.2.1.2. damage to substantia Nigra

4.2.2. Huntington's

4.2.2.1. Inherited AD

4.2.2.2. Degeneration in striatum

4.2.2.3. Loss of GABA neurons

4.2.3. Hemiballism

4.2.3.1. flinging movement of extremities

4.2.3.2. damage to subthalamic nucleus

4.2.4. Wilson's Disease

4.2.4.1. Disorder of copper metabolism

4.2.4.2. damage to lentiform nucleus

5. 4. Types of tremors

5.1. Resting

5.1.1. seen in parkinson's

5.1.2. pill rolling tremor

5.2. Action

5.2.1. Postural

5.2.1.1. Essential

5.2.1.1.1. Most common

5.2.1.1.2. inherited

5.2.1.1.3. improves with alcohol

5.2.1.2. Physiologic

5.2.1.2.1. occurs at any age

5.2.1.2.2. increases by sympathetic stimulation

5.2.1.3. Orthostatic

5.2.1.3.1. unknown cause

5.2.1.3.2. trembling in feet

5.2.2. Intention

5.2.2.1. causes

5.2.2.1.1. cerebellar stroke

5.2.2.1.2. Multiple sclerosis

5.2.2.2. worst with goal directed movements

6. 1. Anatomy

6.1. Basal Nuclei

6.1.1. consists of a number of subcortical nuclei.

6.1.1.1. the putamen

6.1.1.2. globus pallidus externus, and internus

6.1.1.3. the subthalamic nucleus (STN),

6.1.1.3.1. a small collection of neurons situated ventral to the thalamus

6.1.1.4. the substantia nigra (SN).

6.1.1.4.1. region in the midbrain

6.1.1.4.2. a dark appearance

6.1.1.5. Caudate Nucleus

6.1.1.5.1. lateral wall of the lateral ventricle

6.2. Cerebellum

6.2.1. embryonically derived from

6.2.1.1. Metencephalon

6.2.2. Location

6.2.2.1. inferior to the occipital and temporal lobes

6.2.3. lobes

6.2.3.1. the anterior lobe

6.2.3.2. the posterior lobe

6.2.3.3. the flocculonodular lobe.

6.2.4. histology

6.2.4.1. white matter coated by the outer grey

6.2.4.2. cortex

6.2.4.2.1. outer molecular layer,

6.2.4.2.2. the middle layer of Purkinje cells

6.2.4.2.3. the inner granular layer.

6.2.4.3. medulla

6.2.4.3.1. white matter does not contain any cell bodies

7. 5. Diagnosis

7.1. Physical examination

7.1.1. confirming diagnosis

7.1.2. follow ups

7.1.3. Consist of

7.1.3.1. Inspection

7.1.3.2. tests

7.1.3.3. maneuvers

7.1.4. disease's characteristics

7.1.4.1. Bradykinesia

7.1.4.1.1. slowness of movement

7.1.4.1.2. tested by

7.1.4.1.3. Tests

7.1.4.2. Rigidity

7.1.4.2.1. resistance to passive movement

7.1.4.2.2. not direction dependent

7.1.4.2.3. not velocity dependent

7.1.4.2.4. types

7.1.4.2.5. test for

7.1.4.3. Tremor

7.1.4.3.1. involuntary trembling of a body part

7.1.4.3.2. types

7.1.4.4. Gait & Balance abnormalities

7.1.4.4.1. caused by

7.1.4.4.2. tests

7.2. Lab investigation

7.2.1. no test to confirm

7.2.2. to rule out

7.2.2.1. imaging

7.2.2.1.1. stroke

7.2.2.1.2. brain tumor

7.2.2.2. blood test

7.2.2.2.1. thyroid causes

7.2.2.2.2. liver causes

8. Financial burden of healthcare

8.1. Healthcare expenditure determinants

8.1.1. Population

8.1.2. size

8.1.3. structure

8.1.4. epidemiology

8.1.5. growth

8.2. Who pays for the healthcare?

8.2.1. a)Government programs (such as Medicare and Medicaid)

8.2.2. b)Private health insurance plans (some through employers)

8.2.3. c)The person's own funds (out-of-pocket).

8.2.4. Revenue collection

8.2.5. Pooling

8.2.5.1. health risk pooling

8.2.5.2. income pooling

8.2.5.3. age pooling

8.2.6. Purchasing

9. Prognosis of PD

9.1. 1967 – life expectancy = 9.4 years

9.2. 1993 – life expectancy = 13.1 years

9.3. 2016 – life expectancy =14.6 (±7.7) years

10. PD and QoL

10.1. decreased significantly with increased disease severity

10.2. Greatest Impairment in Physical and social functioning

10.3. Decreased across all age groups with greater decrease in younger patients

10.4. Male = female

11. Otitis media complications

11.1. include

11.1.1. Cholesteatoma

11.1.1.1. a small skin cyst

11.1.1.2. 2 types

11.1.1.2.1. Acquired

11.1.1.2.2. Congenital

11.1.1.3. treated by

11.1.1.3.1. Mastoidectomy

11.1.1.3.2. Tympanoplasty

11.1.1.3.3. Ossiculoplasty

11.1.2. Aural polyp

11.1.2.1. growths inside the ear canal

11.1.2.2. may be mimicked by

11.1.2.2.1. Squamous cell carcinoma of ear canal

11.1.3. Tympanosclerosis

11.1.3.1. calcification and hardening of eardrum and middle

11.1.3.2. manifest as

11.1.3.2.1. bright white calcium deposits

11.1.3.3. treated by

11.1.3.3.1. removing sclerotic portions

11.1.3.3.2. Stapesplasty

11.1.3.3.3. hearing aid

12. generalized behavioral changes in a TBI patient

12.1. include

12.1.1. Emotional liability

12.1.1.1. loss of control over their emotional responses

12.1.1.2. include

12.1.1.2.1. alternating between crying and laughing

12.1.1.2.2. not reflect how the person really feels

12.1.2. Apathy

12.1.2.1. reduced emotional expressiveness

12.1.2.2. due to

12.1.2.2.1. lack the ability to show emotions through facial expressions

12.1.3. Egocentricity

12.1.3.1. reduced empathy

12.1.3.2. due to

12.1.3.2.1. lack the ability to interpret social cues

12.1.3.2.2. damage to frontal lobe

12.1.4. PTSD

12.1.4.1. long lasting effects of the trauma

12.1.5. Anxiety

12.1.5.1. usually in noisy environment

12.1.6. Depression

12.1.6.1. struggling with the new disability

12.1.7. Anger

12.1.7.1. from the frustration