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DCCJP > M3 Clinical Neurology > Flashcards

M3 Clinical Neurology Flashcards

1
Q

The bulk of research published within upper cervical chiropractic can generally be found under the following 3 categories;

A
  1. Autonomic Nervous System
  2. cerebellum/basal ganglia / frontal lobe connection
  3. Cranial Nerves
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2
Q

The ANS regulates the three main homeostatic systems in the body. What are they and what chemical messengers does each use?

A
  1. Immune System - cytokines
  2. Endocrine System - hormones
  3. Nervous System - neurotransmitters
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3
Q

Divisions of ANS

A
  1. Sympathetic
  2. Parasympathetic
  3. Enteric
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4
Q

Sympathetic Nervous system

A

Connected to stress response. Drives movement in any form.

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5
Q

Parasympathetic Nervous System

A

Relates to healing and digestion

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6
Q

Enteric Nervous system

A

a mesh-like system of neurons that governs the fn of the gastrointestinal tract. Referred to as 2nd brain.

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7
Q

Polyvagal Theory

A
  1. Developed by Steven Porges in 1991.

2. Proposes two different vagal systems: DVC and VVC

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8
Q

Dorsal Vagal Complex

A 
Unmyelinated
Innervates viscera below diaphragm
Origin: Dorsal Medial Nucleus in Medulla
"Freeze" response
Matures 4th month in utero
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9
Q

Sympathetic Nervous System

A

Movement system
Begins development 16th week in utero
Matures in 3rd trimester
Brakes “Freeze”

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10
Q

Ventral Vagal Complex

A 
Myelinated
Innervates viscera above the diaphragm
Origin: Nucleus Ambiguous in ventral medulla
Begins development in 3rd trimester
Matures at 6th - 12th month
Modulates SNS
Responsible for Social Engagement System
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11
Q

Rostral Ventral Lateral Medulla

A
  1. Sandwiched between DMN and NA

2. Provides governances for SNS

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12
Q

Difference between SNS and PaNS responses.

A

SNS has global response

PaNS has local response

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13
Q

Heart Rate Variability

A

Assesses the function of the VVC.
Respiration is the biggest factor:
1. Inhalation increases SNS, increasing heart rate.
2. Exhalation increases PaNS, decreasing heart rate.
We lose our ability to vary heart rate when there is compromise of the VVC, thus an autonomic imbalance.

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14
Q

Circulation and the SNS

A
  1. Blood pressure and pulse rate are governed primarily by the SNS.
  2. Circulating Norepinephrine will raise or lower pending ANS balance. NE levels rise with sympathetic activation resulting in constriction of the vessels. This drives blood pressure up.
  3. SNS 100% affects the SA Node, regulating pulse rate. The VVC causes it to slow down.
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15
Q

episodes of slow pulse rate, low blood pressure, low blood sugar, passing out, vasovagal responses, etc indicate what?

A

Decreased sympathetic tone, increasing effect of DVC. Can come from poorly developed or exhausted SNS consistent with adrenal fatigue.

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16
Q

Gut and immunity

A
  1. 60-80% of immune system is in gut.
  2. Inflammation in gut can be transmitted to the brain via the vagus nerve.
  3. The gut, as the second brain, is the home of the
    enteric nervous system and can independently drive autonomic function
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17
Q

Typical history of:

Underactive PaNS

A
  • Dry mouth
  • Difficulty swallowing supplements or large bites of food
  • Slow bowel movements/tendency for constipation
  • Chronic digestive complaints
  • Bowel or bladder incontinence
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18
Q

Typical history of:

Overactive SNS

A
  • Tendency for anxiety
  • Easily startled
  • Difficulty relaxing
  • Sensitive to bright or flashing lights
  • Episodes of racing heart
  • Difficulty sleeping
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19
Q

Typical history of:

Weakened SNS response

A
  • Passing out
  • Low blood pressure
  • Low blood sugar
  • Low pulse rate
  • Fatigue
  • Low libido
  • Weight gain
  • Frequent colds/sinusitis
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20
Q

Observation - Pupils

A
  1. The oculomotor nerve (CN III) is a parasympathetic nerve and controls pupil constriction.
  2. Large symmetrical pupils = overactive SNS, normal is infants.
  3. Asymmetrically large pupils are increased on side of weekend hemisphere
  4. Small pupils can indicate a parasympathetic response. (or atrophied ciliary muscles in elderly).
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21
Q

Pupillary Light Reflex

A
  1. The pupil should constrict for 4 to 5 seconds, then gradually lose the constriction and yield. (CN III)
  2. Losing constriction within a couple of seconds or oscillation is positive for a weakened PaNS
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22
Q

ANS and facial symmetry

A

Look for:

  1. deeper nasolabial fold
  2. eye opened wider on one side
  3. drooping lip
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23
Q

ANS balance and temperature

A

Middle finger and wrist should be within 2 degrees F. If finger is cooler then overactive dominance.

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24
Q

ANS balance and fingernails

A

White spots can be banged fingers with decreased blood supply so less healing, therefore SNS dominance.

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25
Q

ANS balance and capillary refill time

A

If it takes longer than 2 seconds for color to return to the patient’s finger, it is considered a slow capillary refill time. This is attributed to decreased circulation and can be an indication of an overactive SNS

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26
Q

ANS balance and orthostatic hypotension

A

BP should increase 10mmHG when standing from laying or sitting. As we stand up, brain stem communicates with the adrenal medulla and the adrenal medulla releases epinephrine and norepinephrine into the system. This causes an immediate increase in blood pressure for the purpose of pushing blood into the cranial vault against gravity. This is a SNS activity. As this system wanes or
weakens orthostatic hypotension can be the result.

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27
Q

ANS balance and Pulse Pressure

A
  1. difference between the systolic pressure and the diastolic pressure. The normal for pulse pressure is 40.
  2. Pulse pressure is an interplay between stroke volume and circulatory resistance.
  3. the most common reason for stiffening of these arteries (elevated pulse pressure) is an overactive SNS activating muscle contraction within these arteries
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28
Q

Testing CN III, IV and VI

A 
Pupillary Light Reflex
Extraocular Movements
1. Look for ptosis, eye position, and nystagmus
2. "H" Pattern
3. Nystagmus testing
4. Accommodation
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29
Q

Testing CN V

A
  1. Test light touch, pain and temperature at forehead, cheeks and chin (pinpoint, not stroking)
  2. Corneal reflex (blinking is CN VII)
  3. mastication muscles
  4. Jaw jerk reflex
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30
Q

Testing CN VII

A
  1. Facial symmetry
  2. Muscles of facial expression
  3. Taste
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31
Q

Testing CN IX

A
  1. Gag response
  2. Uvular deviation (away from affected side)
  3. Palatal articulation “Kah”
  4. Glottal articulation “Go”
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32
Q

Testing CN XI

A
  1. Shrugging shoulders

2. Turning head from side to side

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33
Q

Testing CN XII

A

 Stick out tongue and move it to one side, then the other
 Inspect for tongue atrophy, fasciculations or asymmetry in movement or
appearance

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34
Q

Suggested order of brief CN Nerve exam

A
  1. XII: Stick out tongue.
  2. X/IX: Say “Ah” then gag reflex
  3. VII: raise eyebrows, then puff cheeks, then smile
  4. V: cotton ball for corneal reflex, then forehead, cheeks and chin.
  5. III: observe eyes for PERRLA, convergence,
    smooth pursuits, pupillary reflex
  6. XI: shoulder shrug and head rotation
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35
Q

CNs related to VVC

A

5, 7, 9-12 (3 not related to VVC but important PaNS response).

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36
Q

Which brain hemisphere develops more in first three years of life?

A

Right hemisphere - social engagement side, has mirror neurons to mimic things around and to help intuit others emotions (empathy).

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37
Q

Movement intitiation and refinement loops

A
  1. Motion initiation starts in frontal cortex.
  2. Messages sent simultaneously to:
    a. Basal Ganglia to speed up movement (with thalamus).
    b. Cerebellum: refines movement continuously (8-10 cycles).
  3. Loops connected to the ANS and limbic system.
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38
Q

3 lobes of cerebellum

A

Anterior
Posterior
Flocculonodular

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39
Q

Cerebellar Anterior Lobe

A
  1. a significant portion of the midline cerebellum
  2. houses the fastigual and interpose nuclei
  3. responsible for mediating unconscious proprioception
  4. Inputs are mainly from the spinal cord.
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40
Q

Cerebellar Posterior Lobe

A
  1. houses the dentate nucleus
  2. an important role in fine motor coordination.
  3. receives input mainly from the brainstem (i.e., reticular formation and inferior olivary nucleus) and
    cerebral cortex
  4. This lobe is the lateral most lobe.
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41
Q

Cerebellar Flocculonodular lobe

A
  1. houses the vestibular nucleus
  2. uses information about head movement to influence eye movement and balance.
  3. on the anteroinferior surface of cerebellum and
    connected to the midline structure by thin pedicles
  4. receives inputs from the labyrinthine system. The flocculonodulus is the vestibulocerebellum
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42
Q

4 cerebellar regions

A
  1. flocculonodulus
  2. vermis
  3. paravermis
  4. hemispheres or lateral cerebellum
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43
Q

Cerebellar Vermis

A
  1. most midline structure and houses the fastigual nucleus
    a. Related to the vestibular system
    b. interprets body motion and places it on spatial planes to estimate the movement of the body through space.
    c. large influence on postural muscles, esp spine
  2. Saccadic eye movements
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44
Q

Cerebellar Paravermis

A
  1. Just lateral to vermis
  2. Houses the interpose nuclei:
    a. globus: shoulders and hips
    b. emboliform: elbows to wrists, knees to ankles
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45
Q

Cerebellar Hemispheres

A
  1. Most lateral
  2. Houses dentate nucleus, largest in cerebellum
  3. Related to distal joints: hands and feet
  4. Communicates with cerebrum
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46
Q

3 functional devisions of cerebellum

A
  1. Vestibulocerebellum (flocculonodulus)
  2. Spinocerebellum (vermis and paravermis)
  3. Cerebrocerebellum (lateral hemispheres)
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47
Q

Vestibulocerebellum anatomy

A

Flocculonodular lobe and its connection to the
vestibular and fastigual nucleus. It receives input from the labyrinthine system and the central structures. Since the flocculonodular lobe deals with axial controls and vestibular reflexes, a pathology of this system could give the following disturbances:
• Equilibrium
• Gait ataxia

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48
Q

Vestibulocerebellum lesions

A 
considered midline and the following are possible findings:
A. VOR response
B. Titubation
C. Ataxia of stance
D. Ataxic gait
E. Head tilt
F. Dysarthria
G. Saccadic pursuits
H. Dysmetria of saccades
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49
Q

Spinocerebellar Anatomy

A

Vermal and paravermal regions and their relationship
with the interposed and fastigual nuclei. Receives somatosensory inputs exclusively from the spinal cord. It receives information about the length and tension of muscle fibers (i.e., unconscious proprioceptive sensation).

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50
Q

Spinocerebellar Lesions

A 
A. Gait instability
B. Ataxia in the trunk
C. Titubation and breakdown of movements
D. Saccadic dysmetria
E. Vertiginous activity possibly exocentric or egocentric, depending on the state of the cortex
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51
Q

Cerebrocerebellar Anatomy

A

The lateral hemisphere of the cerebellum receives
information exclusively from the cerebral cortex. It is part of the posterior lobe. Without the cerebrocerebellum the frontal lobe would not expand so
greatly and there would not be the level of lateralization that takes in development. Lateralization is what gives distinction between functions of both hemispheres. It makes the right brain have specific characteristics as well as the left. The distinctions are necessary for higher developed functions seen in human as well as complex cognition.

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52
Q

Cerebellar Peduncles

A
  1. Superior Cerebellar Peduncle (midbrain)
  2. MIddle Cerebellar Peduncle (pons)
  3. Inferior Cerebellar Peduncle (medulla)
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53
Q

Superior Cerebellar Peduncle

A
  • Majority is the interposed and dentate nuclei outputs that go up to the cerebrum
  • Ventral Spinocerebellar tract comes in here
  • Locus ceruleus noradrenergic fibers enter through here
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54
Q

Middle Cerebellar Peduncle

A

Almost exclusively pontocerebellar fibers

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55
Q

Inferior Cerebellar Peduncle

A
  • Olivocerebellar fibers from the contralateral medulla
  • Dorsal spinocerebellar and cuneocerebellar
  • Vestibular afferents, arcuate NU, Trigeminal, raphae serotonergic, reticular afferents and fastigual outputs
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56
Q

The Purkinje System

A
  1. A breaking system for the cerebellum. Without a braking system for the cerebellum there is too much activation for all the areas influenced by each specific nucleus.
  2. Related to mossy and climbing fibers.
  3. Sensitive to oxygenation and other environmental factors.
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57
Q

Sporadic ataxia

A

Ataxia not coming from a known neurological problem.

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58
Q

Mossy fibers

A

Input to cerebellum, primarily activate deep nuclei.

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59
Q

Climbing fibers

A

Activate Purkinje cells, causing deep nuclei inhibition.

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60
Q

Observation of Cerebellar Dysfunction

A
  1. Handwriting - macrografia
  2. Head tilt - away from weak side (and left head tilt may cause writing to slope upwards and right head tilt may cause writing to slope downwards.
  3. Essential tremor
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61
Q

Essential tremor

A
  1. A neurological disorder that causes involuntary and rhythmic shaking. Can be from Cerebellar dysfunction.
  2. Essential tremor most often affects the hands, though it may also affect the head, voice, arms, or legs. It’s not related to Parkinson’s disease.
  3. Shaking occurs with simple tasks such as tying shoelaces, writing, or shaving. Symptoms may be aggravated by stress, fatigue, caffeine, and temperature extremes.
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62
Q

spinocerebellar dysfunction history

A

• Difficulty with balance, or balance that is worse on one side
• A need to hold the handrail or watch each step carefully when going down
stairs
• Feeling unsteady and prone to falling in the dark
• Prone to sway to one side when walking or standing

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63
Q

Spinocerebellar dysfunction exam findings

A
  • Rhomberg’s
  • Wide stance gait
  • Ataxia
  • Instability with ambulation
  • Heel-to-toe walk
64
Q

Vestibulocerebellar dysfunction history

A
  • Episodes of dizziness or disorientation
  • Back muscles that tire quickly when standing or walking
  • Chronic neck or back muscle tightness
  • Nausea, car sickness, or sea sickness
  • A feeling of disorientation or shifting of the environment
  • Crowded places cause anxiety
65
Q

Vestibulocerebellar dysfunction

exam findings

A

• Wide stance gait, ataxia, and instability with ambulation
• Positive Rhomberg’s
• Nystagmus with pure vertical, horizontal, or torsional patterns
• Strabismus and diplopia
• Nystagmus after headshaking test
• Optikinetic activity leads to decay in movement and con induce vertigo
or autonomic symptoms
• Impaired vestibular-ocular-reflex
• Impaired smooth pursuits
• Hypometric and hypermetric saccades
• Findings of dysautonomia during exam including, abnormal HRV

66
Q

Cerebrocerebellar dysfunction

History

A
  • Recent clumsiness in hands
  • Recent clumsiness in feet or frequent tripping
  • A slight had shake when reaching for something at the end of movement
  • Notice shake of utensils before food hits mouth
67
Q

Cerebrocerebellar dysfunction

exam findings

A
  • Intention or kinetic tremor
  • Termination tremor with end-stage targeting (finger-to-nose)
  • Dysmetric (hypometric and hypermetric) targeting (finger-to-nose)
  • Dysdiadokokinesia with rapid alternation movements
  • Ataxia dysarthria
  • Heel-to-shin
  • Hypometric arm swing
  • Finger-to-thumb increased circumference
68
Q

Cerebellar Lifestyle Management

A
  1. Core Strength Exercises - postural muscles that primarily activates the cerebellum
  2. Balance exercises
  3. Metabolic factors -
    a. Neuron basic needs: glucose, oxygen, and activation.
    b. Anemia causes lower oxygen
    c. Blood sugar dysregulation
    d. Oxidative stress
69
Q

Cerebellar cause of sugar dysregulation

A
  1. A failing Purkinje system will not properly gate activation of the deep nuclei.
  2. This results in an excess need for fuel to maintain an overactivated state. Whether that’s nausea with car sickness or anxiety or a panic attack.
  3. The need for more fuel comes at the expense of the blood sugar. These cases can enter a vicious cycle.
    a. Hypoglycemia (low blood sugar) further compromises the Purkinje system and
    b. a compromised Purkinje system further compromises hypoglycemia.
70
Q

Most causes of oxidative stress

A

blood sugar dysregulation
chronic infections
food sensitivities.

71
Q

Gluten Ataxia

A
  1. should be in differential diagnosis of all patients with idiopathic sporadic ataxi.
  2. the amino acid sequence of gliadin (gluten protein) is similar to the amino acid sequence of cerebellar tissue. When a person develops a food sensitivity to gluten the immune system develops IgG antibodies for the attack
72
Q

Toxic elements that can affect CB

A 
 Toluene/benzene derivative
 Aluminum
 Thallium
 Manganese
 Mercury
 Uranium
 Chemical weapons
73
Q

Prescription medications that can affect CB

A
  1. anticonvulsants
  2. antineoplastics
  3. Lithium salts
  4. Amiodarone
74
Q

Hashimoto’s disease and cerebellar dysfunction

A
  1. Hashimoto’s is an autoimmune condition with its target being the thyroid.
  2. The cerebellum is a popular target site for the dysregulated immune system.
  3. Place the patient on an autoimmune protocol.
75
Q

Alcoholic Cerebellar Degeneration

A

Alcohol affects the anterior lobe of the cerebellum much more than any other portion. Much of the spinocerebellum is involved. Easy to see how “impaired driving” tests performed on the side of the road are all spinocerebellar exams.

76
Q

Nutritional Deficiencies and the Cerebellum

A
  1. Vitamine E
  2. Vitamin B-12
  3. Thiamine
77
Q

Basal Ganglia and movement

A
  1. Provides “on” and “off” switch to movement.
  2. The basal ganglia are a series of nuclei that surround the thalamus. The thalamus is connected with the frontal lobe. The basal ganglia either activates or inhibits the thalamus. The thalamus in turn either activates or inhibits frontal lobe movement.
  3. The basal ganglia primarily have two pathways that are referred to as the direct pathway (D1) and the indirect pathway (D2). Each of these pathways has its own receptors.
78
Q

Direct Basal Ganglia Pathway

A

Promotes movement

79
Q

Indirect Basal Ganglia Pathway

A

Inhibits movement

80
Q

Direct Basal Ganglia Pathway Dysfunction

History

A

 Slowness in movements
 Stiffness in muscles (not joints) that goes away during movement
 Cramping in hands when writing
 A stooped posture when walking
 Voice has become softer
 Facial expression changed leading people to frequently ask if you are upset or angry
Also: constipation, micrographia, hx of frozen shoulder

81
Q

Indirect Basal Ganglia Pathway Dysfunction

History

A

 Uncontrolled muscle movements
 Intense need to clear throat regularly or contract a group of muscles
 Obsessive-compulsive tendencies
 Constant nervousness and restless mind

82
Q

micrographia

A

Associated with the breakdown in the basal ganglia direct pathway. Particularly if the end of the sentence has letters smaller than at the beginning of
the sentence.

83
Q

Physical examination findings with basal ganglia direct pathway breakdown

A

 Mask face, reduced blinking, hypophonia, aprosody of speech, resting pill rolling tremor, camptocormia, drooling due to reduced swallowing, slowness of thinking
 Gait analysis demonstrates lack of arm swing, shuffling, slowness, freezing gait, festination, hesitancy initiating first step, limitations of turning, and
postural instability
 Glabellar tap test demonstrating inability to attenuate blinking response after 3 taps
 Pull test – cannot stabilize after 3 steps
 Micrographia and/or tremor with handwriting
 Loss of smell
 Constipation
 Lead-pipe or cogwheel rigidity
 Hypokinetic (bradykinesia) and decrementing movements of limbs with repeated motor tasks (finger-to-thumb, supination/pronation, foot-tapping)

84
Q

Physical examination findings with basal ganglia indirect pathway breakdown

A

 Hyperkinetic movement disorders such as dystonia, hemiballism, chorea, athetosis, restless leg, stereotypy, vocal/motor tics
 Cognitive disorders such as obsessive-compulsive disorder. There are validated OCD questionnaire’s for patients or their parents to fill out. It is a great way to assess improvements, or lack of, in function following the application of upper cervical chiropractic care.

85
Q

clinical red flags for early-stage Parkinson’s

A
  1. Unresolved constipation
  2. history of frozen shoulder without provocation
  3. any of the signs/symptoms/physical exam findings for direct pathway breakdown.

If the clinician observes 2 or three of these, the next step is to perform an odor test.

86
Q

Frontal Lobe function

A

All movement, beyond reflexes, is initiated in the frontal lobe. The frontal lobe, via the prefrontal cortex, houses executive function, social centers and makes us who we are with personality. As a part of brain development, the prefrontal area grows out of the motor area giving movement another essential role. The frontal lobe is intimately connected with the cerebellum. The base of the brain, including the cerebellum drive the developing frontal lobe. This is considered bottom-up development. Once the frontal lobe forms it then reverses roles and exerts control from top-down.

87
Q

Frontal lobe effect on balancing ANS

A

Frontal lobe activation of the brain stem is an important feature for balancing the ANS. In a general sense, the midbrain drives the SNS while the pons and medulla drive the PaNS. Activation from the frontal lobe will have the effect of inhibiting sympathetic tone and activating parasympathetic tone. Remember the VVC originates in the nucleus ambiguous in the medulla. Lack of activation from the frontal lobe can result in an overactive SNS or an under activated PaNS or a combination of both.

88
Q

Basic functions of the frontal lobe

A 
 Planning/goal setting
 Motivation
 Attention
 Reward
 Memory
 Impulse control
 Judgment
 Movement
89
Q

Poor frontal lobe function can lead to:

A

 Depression
 Mental sluggishness and laziness
 Poor impulse control
 Poor social behavior
 Poor handwriting
 Decreased amplitude or slower movements of muscle
 Poor cognitive function, such as poor math or planning skills
 Poor cognitive learning, such as math, new languages, or philosophy
 Poor muscle-coordinated learning such as dancing and playing sports

90
Q

3 distinct regions of the frontal lobe

A
  1. Prefrontal
  2. Motor
  3. Broca’s
91
Q

Prefrontal region function of frontal lobe

A

consists of the prefrontal, dorsolateral and orbitofrontal. These areas direct executive function, personality, motivation social abilities, etc.

92
Q

Motor region function of frontal lobe

A

consists of the supplemental, pre motor and motor

strip

93
Q

Broca’s region function of frontal lobe

A

controls muscles necessary to articulate speech.

94
Q

Prefrontal region of frontal lobe

dysfunction complaints

A

 Difficulty with restraint and controlling impulses or desires
 Emotional instability
 Difficulty planning and organizing
 Difficulty making decisions
 Lack of motivation, enthusiasm, interest, and drive (apathetic)
 Difficulty getting a sound or melody out of your thoughts (perseveration)
 Constantly repeat events or thoughts with difficulty letting go
 Difficulty initiating and finishing tasks
 Episodes of depression
 Mental fatigue
 A decrease in attention span
 Difficulty staying focused and concentrating for extended periods of time
 Difficulty with creativity, imagination, and intuition
 Difficulty in appreciating art and music
 Difficulty with analytical thought
 Difficulty with math, number skills, and time consciousness
 Difficulty taking ideas actions, and words and putting them in a linear sequence

95
Q

Motor region of frontal lobe

dysfunction complaints

A

 Initiating movements with your arm or leg has become more difficult
 Feeling of arm or leg heaviness, especially when tired
 Increased muscle tightness in your arm or leg
 Reduced muscle endurance in your arm or leg
 Noticeable difference in your muscle function or strength from one side to the other
 Noticeable difference in your muscle tightness from one side to the other

96
Q

Broca’s region of frontal lobe

dysfunction complaints

A

 Difficulty producing words verbally, especially when fatigued
 Find the actual act of speaking difficult at times
 Notice word pronunciation and speaking fluency change at times

97
Q

Frontal lobe exams

A 
 Dual tasking
 Gait analysis
 Auditory go no go
 Manual alternating sequence tasking
 Logic and abstraction testing
 Apraxia/dyspraxia
 Spasticity
Of the above list, the top four are exams that can easily be implemented.
98
Q

Neurodegeneration vs

Neurodegenerative Disease

A
  • Neurodegeneration – Loss of neurons or loss of connectivity in specific or generalized areas of the brain
  • Neurodegenerative Disease – Build-up of tau proteins, amyloid bets plaques, alpha-synuclein Lewy bodies leads to distinctive progressive changes in the brain
99
Q

Known causes of dementia

A
  1. Alzheimer’s
  2. Vascular dementia
  3. Dementia with Lewy Bodies
  4. Parkinson’s disease
  5. Frontotemporal dementia
  6. Hypothyroid induced dementia
  7. AIDS dementia complex
  8. Normal pressure hydrocephalus
  9. B12 dementia
  10. Autoimmune dementia
  11. Alcoholic dementia
  12. Drug-abuse dementia
  13. Hormone deficiency
  14. Mixed dementia
100
Q

Alzheimer’s Disease

A

Alzheimer’s is a neurodegenerative disease. At this point, this is not a reversible condition, but we can play an important role in slowing the process. If caught early
enough it is possible the patient can outlive the disease. There are 7 recognized stages of Alzheimer’s. We will do best when we catch people in the 2nd to 4th stage.
Once the condition goes beyond the 4th stage, it is a matter of slowing it down and hoping for the best outcome.

101
Q

Early signs of developing dementia

A

 Forgets recently learned information
 Forgets dates, appointments, and events
 Misplaces keys, wallet/purse, remote control
 Has memory lapses in the middle of a conversation
 Forgets location

102
Q

Physical exam signs for spotting potential developing dementia.

A 
 Gait analysis – arm swing
 Gait analysis – pace
 Dual tasking
 Go-no go
 Manuel alternating sequencing
 Odor test
 Circadian Rhythm – Lab test
103
Q

Odor test

A

To perform the odor test use either coffee, peppermint or anise. These are well-recognized smells. An assistant will be necessary. Use a measuring tape with centimeters (cm). Blindfold the patient and have them close off one nostril. Start at 20 cm’s away. Gradually move the scent closer until the patient says they can smell what you are holding. Record the level in cm’s away from the nostril. Repeat on the other side. According to the above research, the early dementia case will smell the odor 10 cm further away on the right side. Alzheimer’s generally begins on the left side of the brain and affects the olfactory bulb as one of its earliest target sites. The olfactory nerve is ipsilateral, so the left side nostril loses sensitivity first.

104
Q

Dual gait testing

A
  1. early predictor of dementia

2. Gait, or motion testing while simultaneously performing a cognitively demanding task

105
Q

Autophagy

A

This is the process the brain uses to clean up metabolic waste and it mainly occurs during sleeping hours. CSF flow is an essential part of the process.

106
Q

Neurodegenerative processes and lifestyle management

A 
Autophagy and the glymphatic system
Sleep
Exercise
Stress management
Excitotoxins
GI inflammation
Metabolic factors
107
Q

Neurodegenerative processes and autophagy and the glymphatics

A

Tau proteins and beta-amyloid proteins are normally produced in a healthy brain. The neurodegenerative disease brain has issues with producing an overabundance of tau proteins and/or misfolding of the amyloid-beta proteins. The neurodegenerative disease brain may as well not be clearing enough of these detrimental proteins through the cleaning process. The brain is ridded of inflammatory proteins, misfolded protein, and other bad actors through autophagy and the glymphatic system.

108
Q

Neurodegenerative processes and exercise

A

The muscle spindle is the most dominant activator of the brain. According to the neuron theory, a healthy brain must have glucose, oxygen, and activation. Exercise is an important activator of the brain. Exercise that activates the fast-twitch and super-fast twitch muscle fibers shows more benefit in this regard than activation of slow-twitch muscle fibers. Fast-twitch and super-fast twitch muscle fibers are activated by higher intensity workouts.

109
Q

Neurodegenerative processes and excitotoxins

A
  1. a class of chemicals (usually amino acids) that overstimulate neuron receptors. Neuron receptors allow brain cells to communicate with each other, but when they’re exposed to excitotoxins, they fire impulses at such a rapid rate that they become exhausted.
  2. A common excitotoxin is MSG.
  3. Excitotoxins break down neurons.
110
Q

Neurodegenerative processes and GI inflammation

A
  1. Chronic inflammation from the gut can cause chronic inflammation in the brain.
  2. Inflammation can travel up through the vagal root.
  3. The immune system in the brain is called the microglial system. A chronically activated microglial system degenerates the brain at a faster rate than the aging process.
  4. GI inflammation can as well activate the microglial system. When the GI inflammation is chronic, the microglial system can be activated in a chronic state
111
Q

The top three symptoms associated with an inflamed brain

A
  1. fatigue
  2. depression
  3. brain fog.
112
Q

Brain inflammation and concussion

A

Brain inflammation happens post-concussion when the microglial system is activated and it doesn’t shut off. It is most often associated with multiple concussions. Following a concussion there are usually enough antioxidant reserves in-store to calm the brain’s immune response, thus putting out the fire. As the microglial system is back in check normal brain physiology can return. It is repeated blows or an unhealthy antioxidant reserve that allows the microglial system to remain upregulated.

113
Q

The top two causes of gut inflammation are

A

food sensitivities and GI infection.

114
Q

The top five foods people are sensitive to are

A 
 Gluten
 Dairy
 Corn
 Eggs
 Soy
115
Q

Neurodegeneration and oxidative stress

A

Oxidative stress is associated with free radical damage and generally caused by anything that promotes chronic inflammation. From a metabolic standpoint, inflammation is at the epicenter of all chronic degenerative diseases, such as; CVD, diabetes, cancer, Alzheimer’s, Parkinson’s, etc. To have a healthy life and age well, a person must control chronic inflammation.

116
Q

Why does the flocculonodular lobe have a more immediate reaction than the rest of the cerebellum?

A

No nucleus or Purkinje cells.

117
Q

Eye movements - horizontal pursuits

A

mostly Pons

118
Q

Eye movements - vertical pursuits

A

mostly midbrain

119
Q

Eye movements - diagonal pursuits

A

cerebellum

120
Q

Cerebellum and eye movement

A
  1. CB rotates eyes down and to the contralateral side. So diagonal pursuit from upper right to lower left is right CB.
  2. In smooth horizontal pursuit, CB pushes. So a weakness in the Rt CB would cause a saccade on right to left horizontal smooth pursuit.
  3. Ipsilateral CB puts breaks on saccade so as to not overshoot the target, so a fast saccade would indicate a weak ipsilateral CB.
121
Q

Saccade

A

A saccade is a quick, simultaneous movement of both eyes between two or more phases of fixation in the same direction. In contrast, in smooth pursuit movements, the eyes move smoothly instead of in jumps.

122
Q

Basal Ganglia Direct (D1) pathway activator

A

dopamine

123
Q

Basal Ganglia Indirect (D2) pathway activator

A

GABA

124
Q

Caudate Nucleus

A

Part of Basal Ganglia related to emotion and cognition, anything non-motor.

125
Q

Putamen Nucleus

A

Part of Basal Ganglia related to motion.

126
Q

Basal Ganglia parts

A

a group of structures found deep within the cerebral hemispheres. The structures generally included in the basal ganglia are the caudate, putamen, and globus pallidus in the cerebrum, the substantia nigra in the midbrain, and the subthalamic nucleus in the diencephalon.

127
Q

Weight of average brain

A

1500 grams, but with normal CSF flow it only feels like 50 grams (30x less).

128
Q

2nd most physiologically important organ

A

liver

129
Q

Fat makeup of the brain

A

60% of the brain is fat, so gravity can have a great effect on how it sits, especially with damage to stabilization structures.

130
Q

Orbital frontal part of frontal lobe in concussion.

A

Always damaged in a concussion. It manages emotions, motivation, and social behavior. The limbic system is constantly sending it information to manage: anger, hunger, sex. Damage to OF means decreased management of limbic or reptilian brain.

131
Q

CN III dysfunction presentation

A

Impaired adduction, supraadduction, infraadduction of the ipsilateral eye with or without a dilated pupil.
The eye is turned out and slightly down,

132
Q

CN IV dysfunction presentation

A

Eye unable to look down when the eye is looking in towards the nose.

133
Q

CN V dysfunction presentation

A

Ipsilateral alteration of pain, temperature and light touch on the face as far back as the anterior 2/3rds fo the scalp and sparing the angle of the jaw.

134
Q

CN VI dysfunction presentation

A

Ipsilateral weakness of abduction (lateral movement) of the eye.

135
Q

CN VII dysfunction presentation

A

Ipsilateral facial weakness

136
Q

CN VIII dysfunction presentation

A

Ipsilateral deafness

137
Q

CN IX dysfunction presentation

A

ipsilateral loss of pharyngeal sensation.

138
Q

CN X dysfunction presentation

A

ipsilateral palatal weakness

139
Q

CN XI dysfunction presentation

A

ipsilateral weakness of the trapezius and SCM

140
Q

CN XII dysfunction presentation

A

Ipsilateral weakness of the tongue

141
Q

Branches of the facial nerve (CN VII)

A 
Temporal
Zygomatic
Buccal
Mandibular
Cervical
142
Q

Bell’s Palsy vs Supranuclear Facial Nerve Palsy

A

Central nervous system lesions (e.g., multiple sclerosis, stroke, tumor) can also cause facial nerve palsy. However, some motor neurons to the forehead cross sides at the level of the brainstem, so the fibers in the facial nerve going to the forehead come from both cerebral hemispheres. Supranuclear (central) lesions affecting the facial nerve will not paralyze the forehead on the affected side, resulting in a unilateral facial paralysis with forehead sparing. Often, there will be at least some weakness of extremities on the affected side as well.

143
Q

Bell’s Palsy

A

Bell’s palsy is an idiopathic, acute peripheral-nerve palsy involving the facial nerve, which supplies all the muscles of facial expression. The facial nerve also contains parasympathetic fibers to the lacrimal and salivary glands, as well as limited sensory fibers supplying taste to the anterior two-thirds of the tongue

144
Q

Weber test

A

256 or 512 Hz tuning fork on skull vertex.

  1. Normal hearing will produce equal sound in both ears.
  2. Conductive loss will cause the sound to be heard best in the abnormal ear.
  3. Sensorineural loss will cause the sound to be heard best in the normal ear.
145
Q

Rinne Test

A

512 Hz tuning fork placed on mastoid boine, once sound is no longer heard it is placed 1-2cm from auditory canal

  1. Normal hearing will show an air conduction time that is twice as long as the bone conduction time. In other words, you will hear the sound next to your ear twice as long as you will hear the sound behind your ear.
  2. If you have conductive hearing loss, the bone conduction is heard longer than the air conduction sound.
  3. If you have sensorineural hearing loss, air conduction is heard longer than bone conduction, but may not be twice as long.
146
Q

Stages of Brain Development

A
  1. Growth through environment
  2. Segregation and Localization
  3. Integration (vertical and horizontal)
  4. Synchronization
  5. Lateralization
  6. Pruning and refinement
147
Q

Density of muscle spindles per gram of suboccipital muscle tissue

A

242 Inferior Oblique
190 Superior Oblique
98 RCPMajor
98 RCPMinor

148
Q

What is the significance of a lesion of the vestibularcerebellum being midline?

A

When the patient lays down or there is a loss of vestibular influence into the lesion, the patient does not demonstrate any deficits.

149
Q

Titubation

A

s a slow frequency oscillation depending on
postural innervation. Its rhythmicity is, at times, the only
sign distinguishing it from ataxia of the trunk.

150
Q

Brain metabolic profile

A

25% of cardiac output
20% of total body oxygen
25-70% of total body glucose utilization at resting
Starving - ketone bodies

151
Q

Reactive Hypoglycemia presentation

A
  1. crave sweets during the day
  2. irritable if meals are missed
  3. depend on coffee to keep going or get started
  4. gets lightheaded if meals are missed
  5. eating relieves fatigue
  6. Feel shaky, jittery, tremors
  7. agitated easily, upset, nervous
  8. poor memory, forgetful
  9. blurred vision
152
Q

Reactive Hypoglycemia physical exam findings

A
  1. Low blood pressure
  2. orthostatic hypotension
  3. cranial nerve deficits
153
Q

Insulin Resistence presentation

A 
Fatigue after meals
crave sweets during the day
Eating sweets does not relieve craving
Must have sweets after meals
Waist girth is equal or larger than hip girth
Frequent urination
Increased thirst and appetite
Difficulty losing weight
154
Q

Insulin Resistance physical exam findings

A

Blood pressure
pulse pressure
skin tags
acanthosis nigricans

155
Q

Wide stance gait causes suspicion of

A

Early trunk ataxia

156
Q

Celiac disease presentation

A

Cerebellar ataxia
epilepsy
attention/memory impairment
peripheral neuropathy

DCCJP (7 decks)

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