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Brain and Behavior > Exam 2 Deck 2 > Flashcards

Exam 2 Deck 2 Flashcards

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1
Q

Where are the vestibular nuclei locarted?

A

Caudal pons and medulla

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2
Q

Which thalamic nucleus do neurons from the vestibular system that are responsible for the conscious perception of head orientation in space project to?

A

Ventral Posterior (VP) nucleus

This in turn projects to the parietal lobe, immediately posterior to the face area in the primary somatosensory cortex

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3
Q

Which nerves are involved in the afferent limb of the vestibulo-ocular reflex (VOR)?

A

CN VIII (Vestibular nerve from vestibulocochlear) to the medial vestibular nucleus (ipsilateral)

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4
Q

Which nerves are involved in the efferent limb of the vestibulo-ocular reflex (VOR)?

A

CN III, CN VI and the MLF (oculomotor, abducens, medial longintudinal fasciculus)

From vestibular to abducens nucleus. Then goes via MLF to ocolomotor to medial rectus, and to contralateral lateral rectus

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5
Q

Which horizontal canals are activated with head rotation to the right?

A

Right horizontal

Left is inhibited

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6
Q

What are some cerebellum-dependent characteristics of the vestibulo-ocular reflex?

A

Has gain

Is plastic

These features are dependent on the cerebellum

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7
Q

How does caloric testing test the horizontal canals?

A

Nystagmus from reflex

Cold water = nystagmus towards opposite ear

Warm water = nystagmus towards water-injected ear

(COWS)

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8
Q

What is the lateral vestibulospinal tract?

A

Descending motor tract from the vestibular nuclei that is critical for balance and postural control.

Influences motor neurons throughotu the length of the spinal cord (body)

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9
Q

What is the medial vestibulospinal tract?

A

Descending motor tract from teh vestibular nucleus that helps maintain the stability of the head on the necka s teh body moves

Critical in maintaining balance and postural control

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10
Q

What is the course of the lateral vestibulospinal tract?

A

Lateral vestibular nucleus goes to all levels of ipsilateral spinal cord

Receives input from cerebellum

Activates antigravity muscles

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11
Q

What is the course of the medial vestibulo-spinal tract?

A

From medial vestibular nucleus goes bilaterally through MLF to cervical and upper thoracic spinal cord

Activates neck muscles to counteract gravity

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12
Q

What is important about the vestibulocerebellar connections?

A

THE VESTIBULAR NERVE PROJECTS DIRECTLY TO THE CEREBELLUM

All five functional pathways of the vestibular system are under cerebellar control!!

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13
Q

How does the vestibulo-autonomic reflex work?

A

Vestibular nuclei receive primary vestibular input and send projections to the brainstem presympathetic control centers

Here, they converge with the baroreflex

Dysfunction here can cause orthostatic hypotension

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14
Q

How does orthostatic hypotension occur?

A

Dysfunction in the pathway of vestibulo-sympathetic reflex (vestibulo-autonomic)

There is convergence at the point of the presympathetic control centers in the brainstem of vestibular and baroreflex pathways

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15
Q

What is the origin of conductive hearing loss?

A

Outer ear, middle ear

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16
Q

What is the origin of sensory neural hearing loss?

A

inner ear, CNS

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17
Q

What are findings in conductive hearing loss?

A

Air conduction thresholds depressed, bonec onduction thresholds are normal (Air-bone gap)

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18
Q

What are findings in sensoryneural hearing loss?

A

Air and bone conduction are equal. Bilateral

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19
Q

What can cause conductive hearing loss?

A

Ear wax, fluid, eustachian tube swelling, tympanic perforation, cholesteatoma (mass), otosclerosis (fixation of stapes), fusion of bones, congenital, traumatic

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20
Q

What can cause sensory neural hearing loss?

A

Aging - high frequencies first, speech discrimination preserved

Genetic

Noise

Acoustic neuroma

Meniere’s disease

Toxins, virus

Trauma

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21
Q

How do you treat conductive hearing loss?

A

Drainage, surgery

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22
Q

How do you treat sensory neural hearing loss?

A

Surgery, radiation, hearing aid, cochlear implant

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23
Q

How does conductive hearing loss present with tunig fork tests?

A

Sound is perceived louder in the defective ear

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24
Q

How does sensorineural hearing loss present with a tuning fork test?

A

Sound is perceived as louder in normal ear (damaged ear hears less)

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25
Q

What is Rinne?

A

Comparing bone conduction to air conduction

Place tuning fork on mastoid then outside ear

Air should be heard longer/louder than bone (also true in sensorineural loss)

If air heard less than bone - conductive loss

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26
Q

What is vertigo?

A

Vestibular system disease that causes hallucination (false sense) of motion

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27
Q

What is imbalance?

A

Sensory disturbance in vestibular, visual, and/or proprioceptive systems. Can also be cerebellar, motor, etc

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28
Q

What is disequilibrium?

A

Patient feels like things are off balance, drunk

Can be caused by degenerative disorders, brainstem, multisensory, psychogenic

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29
Q

What is lightheadedness?

A

Patient feels like he/she will faint

Usually cardiovascular or metabolic

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30
Q

What is acute unilateral vestibular loss?

A

Sudden onset of vertigo, nausea, vomiting, nystagmus

Positive romberg, past pointing

Ataxic gait, veering towards sesion

Can be casued by virus, trauma, post surgery, infarction

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31
Q

What is Meniere’s syndrome?

A

Episodic vertigo

Spontaneous, unpredictable

History is crucial

lasts for hours

can be perfectly well between episodes

Audiogram is important - unilateral hearing loss

Treat with diuretics, vasodilators, ototoxic drugs on purpose, vestibular suppresants

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32
Q

What is benign positional paroxysmal vertigo (BPPV)?

A

Positional vertigo that lasts for seconds

Caused by canalithiasis (dislodged otoconia that float free in endolymph)

Cured by particle repositioning or surgical ablation

Excellent prognosis with relapses

Diagnose with Dix-Hallpike

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33
Q

What is the Dix-Hallpike maneuver?

A

Diagnostic teset for benign positional paroxysmal vertigo (BPPV)

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34
Q

What is bilateral vestibular loss?

A

presents with ataxia, oscillopsia (perception of oscillating vision)

Not true vertigo

Age related, can be caused by head trauma

Can be caused by drug toxicity or by infection, inflammation or autoimmune causes

Treat with rehab

Poor course

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35
Q

What are causes of central vertigo?

A

CNS Tumors, stroke, migraines, MS

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36
Q

What is central vertigo?

A

Severe imbalance/ataxia

Rarely presents with hearing loss or tinnitus

Can have diploplia, dysarthria and other non-auditory symptoms

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37
Q

What is peripheral vertigo?

A

Ataxia and imbalance that veers towards lesion

Nausea, vomiting, hearing loss, tinnitus, fullness in ear, and pain can be present

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38
Q

What causes peripheral vertigo?

A

Inner ear problems (Semicircular canal issues, otolith issues)

Vestibular nerve problems (BPPV, Meniere’s labyrinthitis)

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39
Q

What is the piriform cortex?

A

Amygdala, Uncus, and Parahippocampal gyrus

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40
Q

What is the role of the thalamus in olfaction?

A

Sensory information does not pass directly to it!

First goes to piriform complex, which sends it to various locations, including the thalamus, secondarily

Sends to Dorsal Medial Nucleus of Thalamus

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41
Q

What are funcitons of the olfactory system?

A

Detection and identification of odorants

Intake regulation

Detection adn avoidance of hazards

Role in sexual behavior

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42
Q

What are som eunique features of the olfactory system?

A

Cell bodies of primary afferents are contained directly in the olfactory epithelium (no ganglia)

Primary afferent neurons undergo continuous turnover (replaced constantly by basal stem cells)

Axons of primary afferents enter the cortex directly (no thalamic relay)

Pathway is entirely ipsilateral

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43
Q

What is special about olfactory epithelium?

A

Contains cell bodies of primary afferents directly!

Has basal stem cells that turnover these primary receptor cells

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44
Q

What are bowman’s glands?

A

Cells in the olfactory epithelium that produce mucus

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45
Q

How does olfactory transduction occur?

A

Odorants are detected at the cilia of the olfactory receptor cells by GPCRs, which leads to an action potential which transduces the signal

GPCR!

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46
Q

How is odor discrimination acheived?

A

Humans have ~400 different odor receptor proteins, and generally speaking each individual olfactory neuron expresses only one type of receptor

They are segregated spatially, which helps for the processing of olfactory bulb information by patterning

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47
Q

What is special about the olfactory tract?

A

They run ipsilateral

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48
Q

What are olfactory glomeruli?

A

Location of first synapse of olfactory cells with mitral cells

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49
Q

What are mitral cells?

A

Cells in the olfactory bulb which will project to the cortex

Many olfactory receptor cells will synapse on a single mitral cell

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50
Q

How does olfaction in humans differ than in other animals?

A

Olfaction is not a strong sense in humans

Other animals have more olfactory receptor neurons and proteins, with expanded olfactory epithelium and a larger portion of the brain devoted to olfaction

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51
Q

What is anosmia?

A

Loss of smell

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52
Q

What is hyposmia?

A

Decreased sensitivity to odorants

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53
Q

What is specific anosmia?

A

Unable to perceive odor of a particular compound or class of compound

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54
Q

What is hyperosmia/olfactory hyperesthesia?

A

Increased olfactory acuity

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55
Q

What is olfactory agnosia?

A

Aware of a smell, but can’t recall name

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56
Q

What is parosmia/dysosmia?

A

Distortion in a smell experience

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57
Q

What is olfactory hallucination/phantosmia?

A

Perception of a smell when no odor is present

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58
Q

What is cacosmia?

A

Formation of repugnant/disagreeable olfactory auras

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59
Q

What can cause anosmia or hyposmia?

A

URI, sinus disease

Head trauma

Tumors

Aging, degenerative diseases

Toxins, medications (smoking, cocaine, chemo)

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60
Q

What can cause hallucinations, cacosmia, or parosmia?

A

Epilepsy

Psychiatric disorders

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61
Q

What can cause hyperosmia?

A

Migraine

Psychosis

Substance abuse

Conversion

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62
Q

What can cause specific anosmia?

A

Genetics/congenital causes

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63
Q

Which cranial nerves contribute to taste?

A

CN VII, IX, X

(Facial, Glossopharyngeal, Vagus)

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64
Q

Where are taste buds found?

A

Tongue, palate, epiglottis, esophagus

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65
Q

What are the 5 categories of tastants?

A

Salt

Sour

Sweet

Bitter

Umami

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66
Q

What is the basis for the differential taste perception of the tongue?

A

All tastes can be detected over the entire surface of teh tongue, but different regions have varying thresholds for each taste

Each tastant category responds to a distinct class of receptor molecules

The taste categories are maintained in the CNS representaitons

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67
Q

What is the structure of taste receptor cells?

A

Distinct apical and basal surfaces (taste receptors on apical surface)

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68
Q

Which tastant categories use GPCR receptors?

A

Sweet, bitter, umami

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69
Q

Which tastant categories use ligand-gated ion channel receptors?

A

Salt, sour

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70
Q

What innervates the anterior 2/3 of the tongue?

A

The facial nerve via the chorda tympani

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71
Q

What innervates the posterior 1/3 of the tongue?

A

The glossopharyngeal nerve

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72
Q

What innervates the taste function of the epiglottis and esophagus?

A

Vagus nerve (CN X)

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73
Q

What is the course of taste sensation?

A

From taste buds to their corresponding cranial nerve

Synapse at the solitary tract nucleus in the brainstem

Here, neurons are projected to the VPM of the thalamus via the central tegmental tract

Then, tertiary neurons project ot the primary gustatory cortex

Discriminative affects of taste and is ipsilateral

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74
Q

What comprises the primary gustatory cortex?

A

Anterior insula and frontal operculum

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75
Q

What is ageusia?

A

Complete loss of taste

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76
Q

What is hypogeusia?

A

Decreased taste sensitivity

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77
Q

What is parageusia/dysgeusia?

A

Unpleasant perception of taste when the substance would normally taste good. Distortion in the perception of taste

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78
Q

What is cacogeusia?

A

Perceptioan of an unpleasant taste sensation

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79
Q

What is gustatory hallucination?

A

Perception of taste when none is present

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80
Q

What can cause taste disturbance?

A

Aging

CN VII lesions

Medications/radiation

Viral medications

Trauma

Diabetes

Seizures

Psychiatric

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81
Q

What are heavy metals that cause neurologic damage?

A

Lead

Mercury

Arsenic

Thallium

Manganese

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82
Q

How does lead poisoning present?

A

Different in children and adults

Children - acute encephalopathy, behavioral and IQ deficits

Adults - abdomina pain and motor neuropathy (wrist drop)

Discoloration of upper gums

Treat with chelators

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83
Q

How does mercury poisoning present?

A

Peripheral neuropathy, seizures, encephalopathy

Mad hatter syndrome

Treat with chelators

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84
Q

How does arsenic poisoning present?

A

Encephalopathy, vomiting, rice water stools, garlic breath, renal failure, arrhythmias

Treat with dimercaprol

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85
Q

How does thallium poisoning present?

A

Hair loss (chronic), vomiting, diarrhea, paresthesia, cognitive impairment

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86
Q

How does manganese poisoning present?

A

Confusion and Parkinsons-like symptoms

Hyperreflexia is an important distinction

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87
Q

What is marasmus?

A

“Balanced starvation”

seen in 0-1 year olds that present with wasting, mental changes, growth retardation

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88
Q

What is kwashiorkor?

A

Protein starvation

Seen in 1-3 year olds that present wiht encephalopathy, muscle wasting

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89
Q

What are neurological complications of obesity?

A

Pickwickian syndrome - Cardiorespiratory distress

Sleep apnea

Can be fatal

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90
Q

What are neurological complications of diabetes?

A

Dementia

Increased stroke risk

Ischemic cranial nerve palsies

Peripheral neuropathies

Loss of limbs (vascular complications)

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91
Q

What is thiamine deficiency?

A

Vitamin B1 deficiency due to impaired intake (seen in alcoholics) or impaired absorption (gastric disorders)

Can cause peripheral neuropathy

Beriberi = peripheral neuritis, symmetrical wasting, no edema

Wernicke’s encephalopathy = ataxia, opthalmoplegia/gaze palsies/nystagmus, confusion

Korsakoff’s psychosis = irreversible with severe memory defecit, confabulation, apathy

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92
Q

What is wernicke’s encephalopathy?

A

Ataxia

Opthalmoplegia/gaze palsies/nystagmus

Confusion

Caused by medial thalamic nuclei, mamillary body, periaqueductal, or brain stem nuclei

Can lead to Korsakoff’s psychosis

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93
Q

What is korsakoff’s psychosis?

A

Irreversible dementia that can be a sequella of wernicke’s encephalopathy

Seen in alcoholics or in thiamine deficiencies

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94
Q

What is pyridoxine deficiency?

A

Vitamin B6 deficiency

Peripheral neuropathy, convulsions, irritability, somnolence

Intractable seizures in infants

Can be induced by isoniazid

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95
Q

What is folic acid deficiency?

A

Vitamin B9 deficiency

Neural tube defects that occur in weeks 3-4 of gestation

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96
Q

What is cobalamin deficiency?

A

Vitamin B12 deficiency

Subacute combined degeneration of posterolateral column

paresthesias, babinski, loss of vibration, position sense, positive romberg, progressive spastic and ataxic weakness, myelopathy….

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97
Q

What is vitamin E deficiency?

A

Progressive spinocerebellar syndrome and posterior column degeneration

Peripheral neuropathy and hemolytic anomia

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98
Q

What are reflexes?

A

Involuntary movement that are the building blocks of purposeful movements.

Mechanoreceptors (sensory) in the skeletal muscle send info to the spinal cord and descending motor information is modified accordingly)

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99
Q

How are rhythmic, complex movements achieved?

A

Combination of involuntary movements (i.e. reflexes) to adjust and compensate coupled with voluntary movements (i.e. purposeful, learned behaviors that require cortical structures) taht initiate the broad movement

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100
Q

What are spinal cord ventral horn motor neurons?

A

Motor neurons with direct acess to muscles

Site of integration of all descending and reflex pathways

(LMN)

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101
Q

What are cranial motor neurons?

A

E.g. facial nucleus, motor nucleus of V

LMN of the cranial nerve system

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102
Q

What are brainstem centers?

A

Nuclei in the brainstem that give rise to descending tracts that are important for postural control (vestibulospinal and reticulospinal tracts)

Under the control of motor cortex and cerebellum

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103
Q

What are the motor cortices?

A

Primary motor cortex (M1)

Premotor area (PM)

Supplementary motor area (SMA)

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104
Q

What is M1?

A

Primary motor cortex

Contains a map of muscles and/or movements and is involved in the execution of the motor plan

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105
Q

What are the premotor and supplementary motor cortex involved in?

A

Planning upcoming movements based on sensory cues or internally generated plans

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106
Q

What are the pyramidal structures of the motor system?

A

Spinal cord ventral horn and cranial motor neurons

Brainstem centers

Motor cortex

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107
Q

What are the extrapyramidal motor system structures?

A

Cerebellum

Basal Ganglia

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108
Q

What is the motor function of the cerebellum?

A

Integrates movements into smooth sequence

May be a comparator between real and intended movement through sensory feedback

May be a motor learning center and in some cases initiator of movement

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109
Q

What is the motor function of basal ganglia?

A

Possibly involved in rapid adjustments of movements (e.g. when turning suddenly)

May initiate some movements

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110
Q

What are the two types of muscle fibers?

A

Extrafusal - force generating

Intrafusal - no direct role in force generation, but part of the spindle (adjust sensitivity)

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111
Q

What are extrafusal muscle fibers?

A

Force-generating muscle fibers

Fast fatigable - glycolysis; pale; strong, but fatigable

Fatigue-resistant/slow - oxidative metabolism; deep red; less strong, but can sustain action

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112
Q

What are intrafusal muscle fibers?

A

Control and adjust the sensitivity of the muscle spindle

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113
Q

What are alpha motor neurons (αMN)?

A

Extrafusal fibers

Fast/fatigable = large

Slow/Fatigue-resistant = small

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114
Q

What are gamma motor neurons (γMN)?

A

Intrafusal muscle fibers

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115
Q

What is a motor unit?

A

The basic contractile unit of skeletal muscle

One motor neuron and all of the muscle fibers it innervates

The ratio of motor neurons to muscle fibers can vary from 1:10 to 1: 2000

A single muscle is composed of many motor units

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116
Q

What is the size principle in motor neuron recruitment?

A

Muscle force is graded by CNS commands that excite increasing numbers of motor units

Large αMNs innervate large, powerful, fast-fatigable muscles and form large motor units

Small αMNs innervate small, weak, non-fatigable muscles and form small motor units

Small αMNs and γMNs are the first to respond to low-level afferents

The largest MNs are the last to be recruited and require strongest afferent stimulation to reach firing threshold

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117
Q

Which are the first muscle fibers to respond to low-level afferent inputs?

A

Small αMNs and γMNs

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118
Q

What is the general layout of motor tracts?

A
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119
Q

How do skeletal muscles monitor changes in muscle length and tension during movement?

A

Muscle spindles are stretch receptors that record length and rate of change of muscles - in parallel with extrafusal muscle fibers

Golgi Tendon Organs (GTO) record tension generated in myotendinous junction during contraction

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120
Q

What are muscle spindles?

A

Feedback mechanism that record muscle length and rate of change

Stretch receptors that are attached with the extrafusal muscle fibers surrounding them

Have two functional regions:

In the central region, which are non contractile, they receive innervation from Group Ia and II sensory afferents

At the polar ends, they are comprised of contractile intrafusal muscle fibers receive motor innervation from γMNs

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121
Q

What are two ways to trigger muscle spindles?

A

Stretch the muscle - will intrinsically activate the Group Ia and II sensory afferents in the central region

Stimulate the γMNs - will contract the polar ends, producing a stretch in the central region, which will activate the sensory afferents.

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122
Q

What is alpha-gamma-coactivation?

A

Phenomenon that occurs during normal contraction during which gamma motor neurons are activated during alpha motor neuron activation as to maintain sensory afferents of muscle length during muscle contraction

Muscle contraction is mediated by extrafusal fibers (alpha motor neurons)

This would produce slack in the muscle, and reduce the sensory afferent signal (by group Ia and II fibers, in the central region), which would result in a lack of information about the length of the muscle

Therefore, intrafusal fibers (gamma motor neurons) fire to “pick up the slack”, keeping a constant tension and maintaining the sensory feedback although the muscle is shortening overall

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123
Q

What are golgi tendon organs (GTOs)?

A

They record the tension generated at the myotendinous junction during contraction

Located at the junction

Composed of Group Ib sensory afferents, interdigitated with surrounding collagen fibers

Encode tension information, but do not generate enough force to create muscle

When muscle creates tension, the fibers are squeezed and stimulates firing

Group Ib fibers stimulate spinal cord interneurons which terminate active muscle contraction and promote opposing contractions

Firing frequencies of the Group Ib fibers are proportional to the degree of force exerted on the myotendinous junction

Increased force = increased GTO recruitment

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124
Q

How are Group Ib fibers activated?

A

They are in the golgi tendon organ

Activated by stretch in muscle which causes impingement of the fibers by collagen

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125
Q

What is a reflex?

A

A motor resopnse to a stimulus and does not normally require volition

Sensory stimulus produces impulses in afferent fibers that subsequently (monosynaptically - direct; or multisynaptically - indirect) activate a pool of motor neurons

Generally, reflex excitation is always accompanied by inhibition

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126
Q

What is a myotatic reflex?

A

A.k.a. Stretch reflex or deep tendon reflex

The things you see in clinic

Stabilizes posture by regulating joint angle

Afferents are made up of Group Ia and II sensory fibers wrapped around muscle spindles

In the spine, alpha motor neurons are activated for the same muscle, and some too for other muscles that are synergistic

Inhibitory interneurons inhibit alpha motor neurons in antagonists

These contract the agonists

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127
Q

What is a homonymous muscle?

A

Same muscle

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128
Q

What is a heteronymous muscle?

A

Muscle that is synergistic to a muscle in question (the homonymous muscle)

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129
Q

What are the intraspinal connections in a myotatic reflex?

A

Group Ia and II sensory afferents synapse on alpha motor neurons of homonymous and to a lesser degree heteronymous muscles

Also activate inhibitory interneurons (Ia inhibitory), which inhibits alpha motor neurons of antagonistic muscles

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130
Q

What is recurrent inhibition?

A

Recurrent axon collaterals feed back to excite inhibitory interneurons (Renshaw cells) which inhibit the alpha motor neurons that initiated the reflex

Self-terminating reflex

Feedback inhibits the alpha motor neuron that recruited it and stops the relaxation of the antagonist muscle by inhibiting the Ia interneurons

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131
Q

What are Renshaw cells?

A

Special inhibitory interneurons that stop the contraction of agonist muscles in a reflex by feeding back to the alpha motor neuron that activated it and by stopping the relaxation of antagonist muscles

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132
Q

What is hyporeflexia and what causes it?

A

Decreased briskness and strength of reflex response

Can be caused by any disease that impairs conduction of action potentials - neuropathies, compression syndromes, motor neuron disease, demyelination, trauma, etc.

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133
Q

What is areflexia and what can cause it?

A

No spinal reflex

Caused by severe disease or injury

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134
Q

What is hyperreflexia?

A

Overly brisk reflexes or exaggerated reflexes

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135
Q

What is the inverse myotatic reflex?

A

Tension-feedback reflex that reduces over-contraction by providing inhibition derived from the Group Ib sensory afferents that innervate the GTOs

Afferent: Group Ib

Intraspinal: Inhibit homonymous alpha MNs and synergists, excite antagonistic alpha MNs

GTOs are recruited in greater numbers as muscle contracts, this activates the reflex and prevents over-contraction

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136
Q

How is purposeful movement achieved?

A

By coordination and modulation of reflexes by descending influences from higher brain centers

All reflexes (except myotatic) operate through interneurons

Ascending pathways provide ongoing sensory information that helps tweak and modulate spinal reflexes and motion

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137
Q

What is lower motor neuron syndrome?

A

Flaccid paralysis that can also have:

Weakness and hypotonia (decreased resistance to passive manipulation)

Areflexia

Muscle atrophy

Fasciculations and fibrillations if the progression is slow

138
Q

What is spinal shock?

A

Phenomenon that occurs in the event of a spinal trauma (e.g. knife wound) where reflexes may be lost or suppressed in lower regions of the spine even though the cord may be intact.

Gradually and variably returns

139
Q

What is the pyramidal tract?

A

Composed of descending cortical fibers which arise from many areas (sensory and motor) of the cerebral cortex.

Only a fraction of the axons will extend to the spinal cord (corticospinal tracts)

The rest terminate in the brainstem nuclei

140
Q

What are corticospinal tracts?

A

Axons in the pyramidal tract which pass through the caudal medulla, crossing in teh pyramidal decussation and form the **lateral corticospinal tract. **

Few remain ipsilateral and form the anterior corticospinal tract which goes to cervical spine then crosses.

141
Q

What are the lateral descending pathways?

A

Lateral and anterior corticospinal tracts

Rubrospinal tract

Target motor neuron pools which control distal muscles and are critical for fine motor control of digits

142
Q

What is the role of lateral group descending tracts?

A

Distal muscles and fine motor control

143
Q

What are the medial descending spinal tracts?

A

Tectospinal tract

Lateral Vestibulospinal tract

Medial Reticulospinal tract

Lateral Reticulospinal Tract

Mostly target motor neuron pools that control axial and proximal muscles and control body posture and reflex adjustments that are imposed by sensory cues (antigravity)

144
Q

How are flexors/extensors and distal/proximal motor functions controlled and located in the spinal cord?

A
145
Q

How is somatopy maintained in the descending cortical motor projections?

A
146
Q

What is the rubrospinal tract?

A

Arises from neurons in the red nucleus

Descending spinal tract (lateral group)

Axons cross completely and descend in the spinal cord in the lateral funiculus just ventral to the lateral corticospinal tract (descends contralaterally)

Axons terminate on contralateral spinal interneurons and facilitate flexor motor neurons and inhibit extensor motor neurons

147
Q

What is the tectospinal tract?

A

Arises from the superior colliculus (tectum)

Axons terminate on spinal interneurons

Facilitates neck rotation (postural reflexes of the head)

148
Q

What are the reticulospinal tracts?

A

Axons originate from teh pontine reticular nuclei = Medial RST

Axons originate from medullary reticular nuclei = Lateral RST

Medial is uncrossed (ipsilateral)

Lateral is bilateral

Have opposite effects

Medial = Extensors of axial muscles

Lateral = Inhibitory effect of axial extensors

149
Q

What is the medial reticulospinal tract?

A

Originates in pons reticular nuclei

Ipsilateral tract that terminates on ipsilateral gamma-motor neurons and interneurons

Helps maintain posture, facilitates axial extensors

150
Q

What is the lateral reticulospinal tract?

A

Axons originate on medullary reticular nuclei

Bilateral tract

Synapse on interneurons

Exerts inhibitory effect on axial extensors; helps maintain posture

151
Q

What is the vestibulospinal tract?

A

Lateral and medial components that arise from the medial and lateral vestibular nuclei in the pons

Lateral runs ipsilateral and synapses on lateral gamma-motor neurons and interneurons

Tonic excitation of axial extensors. Helps maintain posture

Anti-gravity

152
Q

What is the fasciculus proprius?

A

Fiber tract adjacent to the central grey at all levels of the cord that does not send axons beyond spinal cord

Generally forms short interneuon connections that are bilateral in ascending and descending fashion that help coordinate and integrate motor activities at different spinal levels

153
Q

What structures help maintain posture?

A

Brainstem VST (Vestibulospinal tracts), RST (Reticulospinal tracts), cerebral cortex, and cerebellum

154
Q

What provides tonic excitation for the anti-gravity muscles required for posture?

A

Lateral VST and the medial RST

155
Q

What is the inhibitory input that balances tonic excitation of the anti-gravity muscles?

A

Purkinje cells in the cerebellum inhibit lateral VST

Cerebral cortex provides stimulation to the lateral RST which inhibits extensor motor neurons

156
Q

What is the decerebrate rigidity model?

A

Correlates to spasticity clinically

Brainstem-transected cats demonstrate excessive hypertonia of extensor anti-gravity musculature

Knocks out cortical input to Lateral RST. This results in unbalanced activity of gamma-motor neurons which maintains the hypertonic state via a persistent myotatic reflex

Can be alleviated by lesioning DRGs

157
Q

What is hypertonia?

A

Increased resistance to passive limb manipulation

158
Q

What is rigidity?

A

Damage to structures of the basal ganglia; hallmark of Parkinson’s disease

Symptoms include hypoactive myotatic reflexes

Hypertonia throughout extensors and flexors

Cog-wheel type resistance

159
Q

What is the primary motor cortex?

A

M1 area 4

Focused with motor execution

Cells discharge immediately before movement.

Organized into humunculus

Organized into interconnected cortical columns

Strictly contralateral

Small cells - delicate movements

Large cells - ballistic movements

Caudal precentral gyrus into anterior bank of central sulcus

160
Q

What are features common to all motor cortical areas?

A

Neurons become active prior to movement onset

They have a low threshold of excitability

They have a small layer IV of cortex (large layer V)

Have corticospinal and other connections

Have thalamic inputs (from VLp and VLa)

161
Q

Which neurons in the motor cortex are most immediately related to aspects of motor execution?

A

M1

162
Q

How are primary motor cortex neurons organized?

A

Into heavily interconnected columns of elementary movements which can be recruited in different repertoires according to the motor task required

163
Q

Where are corticospinal neurons located in the motor cortex?

A

Layer V

164
Q

What are characteristics of the large corticospinal neurons of the motor cortex?

A

Betz cells

Concerned with ballistic bidirectional movements

Show all or none firing

Not influenced by sensory feedback

10% of pyramidal tract axons

165
Q

What are characteristics of small corticospinal neurons of the motor cortex?

A

Concerned with slow, accurate, controlled movements

Unidirectional movement

Tight somatosensory feedback control

Graded firing potential to force exerted

90%

Majority synapse to interneurons

166
Q

Which motor cortex cells are responsible for large, ballistic movements?

A

Betz cells (Large cells) of the corticospinal neurons

167
Q

What cells of the motor cortex are responsible for slow, accurate, delicate, directionally selective movements?

A

Small corticospinal neurons

168
Q

What are characteristics of the premotor cortex and the supplementary motor area?

A

Instruct M1

Involved in motor preparation and planning

Discharge before M1

169
Q

What side of the body do M1 neurons correspond to?

A

contralateral

170
Q

What side of the body do premotor cortex neurons correspond to?

A

Contralateral, mostly but some bilateral

171
Q

What side of the body do supplementary motor area neurons correspond to?

A

Bilateral

172
Q

What is the function of premotor cortex neurons?

A

Sensory guided movement planning (e.g. reaching for a target in extrapersonal space based on sensory cues that dictate the movement)

173
Q

What is the function of supplementary motor area neurons?

A

Guide internally generated movement planning

Especially for movements involving bimanual coordination

Activate upon even thinking about a movement, not just before the actual movement

174
Q

Which lesions can present with upper motor neuron damage?

A

Damage to the coritcal areas, internal capsule, or pyramidal tract

175
Q

What are some signs/symptoms of UMN lesions?

A

Weakness

Spasticity (hypertonus of extensor muscles and flexors of forearm

Clasp-knife response to passive manipulation of limbs

Babinski sign

Atrophy of muscle

176
Q

What are some signs/symptoms of LMN lesions?

A

Weakness

Areflexia

Flaccid paralysis

Pronounced muscular atrophy

177
Q

What additional impairments do you see in M1 lesions (apart from UMN)

A

Permanent loss of fine motor control including loss of independent finger movements

178
Q

What additional impairments do you see in PM cortex lesions (apart from UMN)?

A

Severe impairment in performing sensory-guided motor tasks

179
Q

What additional deficits do you see in SMA lesions (apart from UMN)

A

Impairment in performing self-initiated motor tasks and especially in those that require bimanual coordination.

Leads to forced grasping (difficulty letting go of objects)

180
Q

What are the components of a motor exam?

A

Observation and palpation - gait, inspection fo muscles for symmetry, loss of bulk, atrophy, and fasciculations

Tone and Power - 0 to 5 scale (3 is against gravity)

Reflexes - absent to hyperreactive scale (0 to 4, 2 is normal)

181
Q

What is the distribution of weakness in upper motor neuron lesions?

A

Upper extremities: Flex stronger than extensors

Lower extremities: Exntensors stronger than flex

182
Q

What is hemiplegic gait?

A

Arm is held in flexion with marked weakness of extensors of fingers, wrist, shoulder

Hand and fingers are tightly clenched.

Outward swinging of leg and reduced armswing

UMN

183
Q

What is spastic gait?

A

Toe walking

Slow, stilff, walking with small steps

Hyperreflexia, clonus and positive babinski

UMN

184
Q

What is frontal (magnetic) gait?

A

Seen in normal pressure hydrocephalus

Problems getting out of chair and finging center of gravity

Walk as if feet stuck to ground

hyperreflexia, plantar response, but minimal weakness

185
Q

What is ALS?

A

Both UMN and LMN abnormalities

Bulbar palsy - dysarthria, dysphagia, impaired jaw-jerk, tongue fasciculations

pseudobulbar palsy - emotional swings

Preservation of extraocular muscles with no cognitive or sensory changes

Pelvic floor muscles/sphincters spared

MUST demonstrate disease above foramen magnum to differentiate from other disorders

Poor prognosis

186
Q

What is primary lateral sclerosis?

A

Similar to ALS but only involves UMN

Abscence of cognitive, LMN or sensory involvement and nof family history

187
Q

What is Guillain-Barre syndrome?

A

Acute autoimmune polyneuropathy

MS of the PNS

Often follows infection (campylobacter jejuni is common)

Facial weakness, difficulty breathing, pain

Lost reflexes with weakness

Medical emergency

188
Q

What are common presentations in peripheral neuropathy?

A

Distal weakness - longest nerves first

Steppage gait - LMN leg weakness due to distal muscles

Foot drop - weak ankle dorsiflexion

Weakness, hyporeflexia

189
Q

What organism is Guillain-Barre syndrome associated with?

A

Campylobacter jejuni

190
Q

What is steppage gait?

A

LMN leg weakness where the patient slaps foot on the floor because they make a conscious effort to raise the foot as to not drag it.

191
Q

What are some presentations of myopathies?

A

Proximal weakness with normal sensation, sphincter function and preservation of reflexes

Gower’s sign - hard to climb up

192
Q

What is myotonia?

A

Disorder of muscle membrane (channeloopathy)

Slow relaxation of muscles after voluntary contraction

Improved upon warming of muscles

193
Q

What is botulism?

A

Toxin from clostridium botulinum

Infants present with floppy baby

194
Q

What causes floppy baby?

A

C. botulinum spores (botulism)

195
Q

What is tick paralysis?

A

Caused by neurotoxin in tick salivary gland that may look like Guillain Barre

Ascenidng paralysis and respiratory fialure. Reflexes decreased

196
Q

What is ciguatera toxin?

A

Caused by injesting certain fish

Toxin from a seaweed

Patients develop nausea, vomiting, weakness, muscular cramps, metallic taste, paralysis, coma, respiratory fialure

197
Q

What is monoplegia?

A

Paralysis of one limb

198
Q

What is diplegia?

A

paralysis of both upper or lower limbs

199
Q

What is paraplegia?

A

paralysis of both lower limbs

200
Q

What is hemiplegia?

A

Paralysis of upper limb, torso, and lower leg on one side of body

201
Q

What is quadriplegia?

A

paralysis of all four limbs

202
Q

What are basic findings in spinal cord disease?

A

UMN findings below the sign (hyperreflexia and Babinski)

Sensory and motor involvement that localizes to a spinal cord level

Bowel and bladder dysfunction

Recall, spinal cord ends at T12-L1

203
Q

What can cause a compressive myelopathy?

A

Spondylolisthesis - dislacement of vertebrae

Tumor

Abscess

Disc prolapse

Spinal shock

204
Q

What are the dermatome landmarks?

A
205
Q

What is Syringobulbia?

A

Syrinx that affects the brainstem - results from congenital, tumor, or trauma

May affect cranial nerves and cause facial palsies

206
Q

What do you see in complete spinal cord transections?

A

All ascending tracts from below and all descending tracts from above will be interrupted

Caused by tumor, MS, viruses, vascular, autoimmune, herniated disk

Paraplegia, quadriplegia

207
Q

What is Brown-Sequard syndrome?

A

Ipsilateral UMN, mechanosensation deficits below the lesion

Contralateral pain/temp deficits below lesion

At lesion - ipsilateral LMN deficits, ipsilateral loss of all sensation

If lesion is above T1 = horners

Normal bladder/bowel

208
Q

What is central cord syndrome?

A

Usually invovles cervical lesion (classic is cervical spondylosis with a hyperextension injury)

Damage ot anterior white commisure, spinothalamic tract

Bilateral pain and temp loss, preserved mechanosensation

Similar to syringomyelia or syringobulba

209
Q

What is posterolateral column disease?

A

Subacute demyelination of dorsal columns, lateral corticospinal tract, spinocerebellar tract

UMN issues

Parestheisas of hands and feet

Positive romberg

Can be caused by B12 deficiency, Vit. E deficiency. Vacuolar myelopathy (AIDS, HTLV-1, tropical spastic paraparesis)

210
Q

What is is Conus Medullaris Syndrome?

A

Sudden onset with bilateral presentation

L1, L2 level of cord

Causes minimal symmetric weakness

Causes symmetric saddle anesthesia, pain is not prominent

LMN bladder and bowel dysfunction develops early

211
Q

What is Cauda Equina Syndrome?

A

Gradual onset, with asymmetric presentation

At the level of L4, L5, S1 nerve roots

Flaccid paralysis, hypotonia, areflexia

Asymmetric saddle amnesia with radicular pain - painful

Decreased rectal tone

LMN bladder/bowel issues develop late

212
Q

What occurs in disc prolapse?

A

Spinal cord/nerve root compression - most common are C or L spine

Radiculopathy - sharp shooting pain

Numbness, weakness, bowel/bladdre disruption

213
Q

What is spondylolisthesis?

A

Anterior-posterior slippage of the vertebrae

214
Q

What is tabes dorsalis?

A

From Tertiary syphylis in which nerves of dorsal columns degenerate

Loss of sense of position, vibration, discriminative touch

Locomotor ataxia

Positive Romberg

Argyll Robertson pupils

215
Q

What is an epidural abscess?

A

Rare infection (staph) that causes spinal cord/root compression

Back pain, radiculopathy are common

Need surgery and antibiotics

216
Q

What organism commonly causes epidural abscesses?

A

Staph aureus

Common in immunosuppressed patients

217
Q

What are the three classifications of tumors of the spinal cord?

A

Extradural (epidural) = most

Intradural extramedullary (in meninges)

Intramedullary (inside cord)

218
Q

What is the more common origin of spinal cord tumors?

A

Metastatic - breast, prostate

219
Q

What can cause an anterior spinal cord injury?

A

Anterior spinal artery infarct

220
Q

What is anterior cord syndrome?

A

Caused by vascular injury

Bilateral loss of motor control, pain temperature

Preserved mechanosensation

Below T8 is less common because of Artery of Adamkiewicz

221
Q

What is the watershed area of vascular disease of the spinal cord?

A

Above T8 (upper thoracic)

Below T8 you have Artery of Adamkiewicz to supply blood

222
Q

What brainstem lesions affect descending motor pathways?

A

Anterior (ventral)

223
Q

What brainstem lesions affect ascending sensory pathways?

A

Posterior (dorsal)

224
Q

What is the hallmark of a brainstem lesion?

A

Crossed signs!!!

Lesions to CN cause symptoms on one side of the face

Lesions to the ascending or descending pathways cause symptoms on the other side of the body

225
Q

What is Weber syndrome?

A

Lesions of the midbrain that affect CN III and the corticospinal tract

Caused by PCA blockages

Presents with diploplia, down and out eye (ipsilateral), ptosis

Contralateral hemiplegia

226
Q

Patient presents with double vision, with right eye that doesn’t abduct. Has left sided weakness and trouble walking. Where is the lesion/

A

Anterior Pons

Affects CN VI and corticospinal tract

Blockages of Basilar artery

227
Q

What is Millard-Gubler syndrome?

A

Lesions of the pons that affect CN VI, VII (and sympathetics), and the corticospinal tract

Basilar arteries usually involved

Ipsilateral facial palsy, lack of abduction, decreased corneal reflex, tear secretion, contralateral hemiplegia

228
Q

What is Wallenberg Syndrome?

A

Lateral medulla lesion (caused by vertebral artery, PICA)

Affects CN V, spinothalamic tract, Nucleus ambiguous (9-11), vestibular nucleus, descending sympathetics from hypothalamus

loss of pain in ipsilateral face, contralateral body

Hoarse voice, dysphagia, dysarthria, decreased gag

Nystagmus, nausea/vomiting, vertigo, gait ataxia

Horner syndrome

229
Q

What is Jackson Syndrome?

A

Ventral, medial medulla lesions

Affect CN XII, corticospinal tract

Issues with anterior spinal artery

Present with dysarthria with lingual quality. Hemiatrophy of trongue. Contralateral hemiplegia

230
Q

What is Locked-in Syndrome?

A

Bilateral lesion of anterior pons

Affects corticospinal and corticobulbar tracts, CN VI, MLF

Spares CN III

Caused by basilar artery stroke, central pontine myelinosis

Patients present quadriplegic, aphonic, no horizontal eye movement, but can blink

Are conscious!

231
Q

What are lesions of the lateral medulla called?

A

Wallenberg Syndrome!!!

Caused by vertebral artery or PICA infarcts

Loss of pain in ipsilateral face, contralateral body

Hoarse voice, dysphagia, dysarthria, decreased gag

Nystagmus, nausea, vomiting, gait ataxia,

Horner’s

232
Q

What is the function of the cerebellum?

A

Key structure for motor learning and coordination

233
Q

What is the main symptom of cerebellar damage?

A

Ataxia - issues synthesizing smooth, well-timed and proportional movements

234
Q

What are the cerebellar lobes?

A

Anterior, posterior, flocculonodular

235
Q

What are the Identify the anterior lobe of the cerebellum.

A
236
Q

Identify the posterior lobe of the cerebellum

A
237
Q

Identify the flocculonodular lobe of the cerebellum

A
238
Q

What is a folium?

A

Equivalent to a gyrus in the cerebellum

239
Q

What is a cerebellar lobule?

A

A combination of multiple folia in the cerebellum

240
Q

Identify the primary fissure of the cerebellum

A
241
Q

Identify the postero-lateral fissure of the cerebellum.

A
242
Q

Idnetify the horizontal fissure of the cerebellum

A
243
Q

What connections pass through the inferior cerebellar peduncle?

A

Connections fromthe medulla and spinal cord to the cerebellum

244
Q

What information passes through the middle cerebellar peduncle?

A

Connections from the pontine nuclei to the cerebellum

245
Q

What information passes through the superior cerebellar peduncle?

A

Exiting efferents from the cerebellum (except vestibular), and afferent ventral spinocerebellar tract axons

246
Q

Where is the fastigial nucleus found?

A

In the vermis

247
Q

Where is the interposed nucleus found?

A

Between fastigial and dentate nucleus

248
Q

Where is the dentate nucleus found?

A

Lateral cerebellum

249
Q

Identify the fastigial nucleus

A
250
Q

Identify the interposed nucleus

A
251
Q

Identify the dentate nucleus

A
252
Q

What is the spinocerebellum?

A

Vermis and intermediate hemisphere

Contains somatotopic representations of the head nad body and sends efferents to spinal motor nuclear tracts

253
Q

Which part of the spinocerebellum receives axial body input and projects through medial descending motor systems?

A

Vermis

254
Q

Which part of the spinocerebellum receives distal body inputs and projects through lateral descending systems?

A

Paravermis (intermediate hemisphere sections)

255
Q

What are the lateral hemispheres of the cerebellum responsible for?

A

Cerebrocerebellum - receive input from cerebral cortex via the pontine nuclei and do not receive direct somatosensory input

256
Q

What is the flocculonodular lobe of the cerebellum responsible for?

A

The vestibular cerebellum.

Connectivity breaks all the rules of the other cerebellar structures

257
Q

What is the part of the cerebellum responsible for vestibular functions?

A

flocculonodular lobe

258
Q

What are the four spinocerebellar tracts?

A

Dorsal spinocerebellar tract - lower boddy proprioception

Ventral spinocerebellar tract - lower boddy error signal

Cuneocerebellar tract - upper body proprioception

Rostra spinocerebellar tract - upper body error signal

259
Q

Which spinocerebellar tracts are involved with proprioception?

A

Cuneocerebellar tract (upper body)

Dorsal spinocerebellar tract (lower body)

260
Q

Which spinocerebellar tracts are involved with transmitting error signals?

A

Rostral spinocerebellar tract (upper body)

Ventral spinocerebellar tract (lower body)

261
Q

Which spinocerebellar tracts go to the lower body?

A

Dorsal and ventral spinocerebellar tracts

dorsal = proprioception; ventral = error signal

262
Q

Which spinocerebellar tracts go to the upper body?

A

Cuneocerebellar tract = proprioception

Rostral spinocerebellar tract = error signal

263
Q

What is the dorsal spinocerebellar tract?

A

Ipsilateral lower body proprioceptive tract

Muscle spindle afferents carry proprioception from lower body climb up the fasciculus gracilus and terminate in Clarke’s nucleus. Project through ipsilateral dorsolateral funiculus and inferior cerebellar peduncle to the intermediate zone of cerebellum

264
Q

What is the cuneocerebellar tracts?

A

Proprioceptive upper body spinocerebellar tract

Ipsilateral

Muscle spindle afferents carry proprioceptive info to external cuneate nucleus. These axons travel up with teh dorsal spinocerebellar tract and end in intermediate zone of cerebellar cortex

265
Q

What is the ventral spinocerebellar tract?

A

Lower body error signal spinocerebellar tract

Contralateral ascent, re-cross in cerebellum

GTO afferents project to spinal interneurons. Cross in spinal cord and ascend in the ventrolateral funiculus

Travel through superior cerebellar peduncle and recross midline

Cerebellar projection is ipsilateral

266
Q

What is the rostral spinocerebellar tract?

A

Upper body error signal tract

GTO to interneurons through inferior cerebellar peduncle to cerebellum

267
Q

Which spinocerebellar tracts course through the inferior cerebellar peduncle?

A

Cuneocerebellar, dorsal spinocerebellar, rostral spinocerebellar

Ventral spinocerebellar courses through the superior cerebellar peduncle

268
Q

Which spinocerebellar tract courses through the superior cerebellar peduncle?

A

Ventral spinocerebellar tract

Dorsal, cuneocerebellar, and rostral course through inferior peduncle

269
Q

What are the inputs to the cerebellum?

A

Spinocerebellar tracts (4 of them)

Reticular formation

Vestibular nerve, nuclei

Pontine nuclei

Inferior olivary complex

270
Q

What are the layers of the cerebellar cortex?

A

Molecular = closest to pia

Purkinje = middle

Granular = deepest

271
Q

Which cells are the key to the cerebellar cortex?

A

Purkinje cells

Reside in the purkinje layer

GABAergic, inhibitory neurons

272
Q

What cells reside in the molecular layer?

A

Purkinje cell apical dendritic trees (perpendicular to long axis)

Climing fiber axon terminals - which provide direct, convergent input to purkinje cells

Stellate cells = inhibitory interneurons to Purkinje dendrites

Basket cells = inhibitory interneurons to Purkinje cell bodies

Excitatory parallel fibers (course parallel to long axis)

273
Q

What are the climbing fibers?

A

Synapse directly to Purkinje cells and arise from the Inferior Olivary Complex

Provide convergent excitation (one purkinje cell receives input from one climbing fiber; but each climbing fiber innervates only a few Purkinje cells; however, the climbing fibers make thousands of synapses on each Purkinje)

274
Q

What are mossy fibers?

A

Provide input from all sources except inferior olivary complex

Provide indirect input to purkinje cells. Relayed via parallel fibers of granule cells located in glomeruli

These convey excitatory information to large number of Purkinje cells

275
Q

What is a cerebellar glomerulus?

A

Located in granular layer

Comprised of mossy fiber axon terminal (excitatory; Golgi cell axon terminal (inhibitory) and several post-synaptic granule cell dendrites

276
Q

Describe the inputs of cerebellar cortex

A
277
Q

What are the outputs of the cerebellar cortex?

A

Purkinje cell is the only output

Project to cerebellar nuclei or to the vestibular cerebellum

278
Q

How doe the cerebellum control pusture?

A

Flocculonodular lobe and vermis project to the vestibular nuclei of the brainstem (bilaterally) with no cerebellar relay. From here goes to reticulospinal and vestibulospinal tracts to the axial, neck muscles

Some vermis projections to the vestibular nuclei relay through the fastigial nucleus

279
Q

How does the cerebellum control motor control?

A

Paravermis nuclei (interposed nuclei = globulose and emboliform nuclei) project through the superior cerebellar peduncle to the contralateral red nucleus (decussates)

Activate rubro-olivary tract (red nucleus to inf. olivary complex, to cerebellar peduncle and climbing fibers)

Activate rubrospinal tract (red nucleus to midbrain decussation to distal misculature)

280
Q

How does the cerebellum control motor planning?

A

Lateral hemispheres of the cerebellum project to the dentate nuclei which send axons through superior cerebellar peduncle to the VLp in the thalamus (contralateral). These go to the cerebral cortex which send projections to the distal musculature through corticospinal tract

Dentate nuclei also project to red nucleus , which lets the red nucleus integrate info from paravermal intermediate zone and lateral hemispheres

281
Q

Why are cerebellar deficits always ipsilateral to the lesion?

A

All outpus (except vestibular) course through the superior cerebellar peduncle. This decussates as it ascends and targets the red nucleus and cerebellar cortex through the thalamus. The resulting descending tracts also cross (back) to the muscles of the ipsilateral side of the lesion

282
Q

What are cardinal features of cerebellar dysfunction?

A

Ataxia

Decomposition of movement

Dysarthria

Dysdiadochokinesea

Dysmetria

Hypotonia
Nystagmus

Scanning Speech

Tremor

283
Q

What is ataxia?

A

Reeling, or wide-based gait

284
Q

What is decomposition of movement?

A

Inability to correctly sequence fine coordinated acts

285
Q

What is dysarthria?

A

Inability to articulate words correctly with slurring and inappropriate phrasing

286
Q

What is dysdiadochokinesia?

A

Inability to perform rapid altering movements

287
Q

What is dysmetria?

A

Inability to control range of movement (abnormal trajectories through space)

288
Q

What is hypotonia?

A

Decreased muscle tone

289
Q

What is scanning speech??

A

Slow enunciation with a tendency to hesitate at the beginning of a word or syllable

290
Q

What is tremor?

A

Rhythmic, alternating, oscillatory movement of a limb as it approaches a target (intention tremor)

291
Q

What are features of Vermis Syndromes?

A

Symptoms that affect the trunk

Wide-based gait and stance

Truncal titubations (staggering)

Arm and leg coordination are spared

Gait abnromalities not improved by visual orientation (indiscriminate falling)

Eye movement disturbances

Rotated postures of head

Test by tandem toe-heel walking; walking backwards; hop on each foot; romberg

292
Q

What is the most common cause of midline (vermis) cerebellar syndromes?

A

Chronic alcohol use

293
Q

What are symptoms of hemispheric cerebellar syndromes?

A

Appendicular ataxia - loss of coordination of limbs ipsilateral to lesion

Impaired rapid alternating movements

Gait abnormalities not improved by visual orientation - fall toward lesion

Dysdiadochokinesia, Dysarthria, Dysmetria

Tremors

Hypotonia

Test with rapidly alternating movements (finger to nose, heel-knee-shin), check and rebound, past pointing

294
Q

What are common causes of cerebellar hemisphereic syndromes?

A

Metastasis, infarcts, abcesses

295
Q

What are pancerebellar syndromes?

A

Combination of vermis and hemispheric syndromes

Can be caused by infectious processes, hypoglycemia, paraneoplastic disorders, drunkenness

296
Q

What oculomotor dysfunctions are commonly seen in cerebellar disorders?

A

Nystagmus (gaze evoked, upbeat, rebound)

297
Q

What is the Romberg Sign?

A

Close eyes and stand still

Patients will fall with both cerebellar and posterior column disease

With eyes open, patients with cerebellar disease will fall.

Posterior column defecits will present with eyes closed (falling out of shower)

298
Q

What do cerebellar tremors present as?

A

Intention tremors

Occur during purposeful/directed movement (especially near end)

Usually slow frequency, coarse, and broad

299
Q

What do non-cerebellar tremors present as?

A

Resting tremors, usually

Occur maximally at rest and decrease with activity

300
Q

What structures are likely affected in a patient with a resting tremor that improves with motion?

A

Not cerebellum!

301
Q

What structure is likely affected in a patient with a tremor that worsens with movement and is worse at the end of a movement towards an object?

A

Cerebellum!

302
Q

What is a resting tremor?

A

Maximal at rest

Decreases with activity

Usually symptom of Parkinson’s

303
Q

What is a postural tremor?

A

Maximal with limb in a fixed position against gravity

Gradual onset suggests physioloic or essential tremmor

Acute onset suggests toxic/metabolic disorder

304
Q

What is an intention tremor?

A

Maximal during movement toward a target (finger to nose)

Suggests cerebellar disorder but may be due to somethign else (MS, Wilson’s)

305
Q

What is asterixis?

A

Flapping “tremor” in wrist due to liver failure (think metabolic)

Caused by interruptions of contraction in wrist extensors

306
Q

What is a pill-rolling tremor indicative of?

A

Parkinsons!

307
Q

What do dysfunctions of the basal ganglia present as?

A

Motor behavior and reward seeking deficits

Tremor, rigidity, dyskinesias, loss of postural reflexes, chorea, ballismus, dystonia, addiction

Parkinson’s, Huntingtons, Tourette’s, hemibalismus are diseases

308
Q

What are the components of the basal ganglia system?

A

Striatum (dorsal = caudate nucleus + putamen; ventral = nucleus accumbens septi)

Pallidum (external, internal, ventral)

Substantia nigra (compacta, reticulata)

Ventral tegmental area

Subthalamic nucleus

309
Q

What are the major inputs to the basal ganglia system?

A

Cerebral cortex (huge) - glutamatergic

Thalamus - glutamatergic

Midbrain - dopaminergic

Raphe nuclei - serotinergic

Locus ceruleus - noerepinephrine

310
Q

How is cerebral cortical input to the basal ganglia organized?

A

Topographically

from all areas, but especially the frontal lobe

311
Q

Where does thalamic input to the basal ganglia originate from?

A

Ventral group (VA/VM; VLa)

Inrtralaminar nuclei (CM)

Medial Dorsal Nucleus (MD)

312
Q

What are the main efferent cells of the striatum?

A

Medium Spiny Neurons (GABA-ergic)

313
Q

What are the two subtypes of the medium spiny neurons of the striatum?

A

Substance-P colocalizing neurons with D1 receptors (excitatory)

Enkephalin colocalizing neurons with D2 receptors (inhibitory)

Project to Globus Pallidus and Substantia Nigra

314
Q

What are the components of the striatum?

A

Dorsal = caudate and putamen

Ventral = nucleus accumbens septi, olfactory tubercule

315
Q

What is the dorsal striatum?

A

Putamen and caudate nucleus

316
Q

What is the ventral striatum?

A

Nucleus accumbens and olfactory tubercule

317
Q

What is the subthalamic nucleus?

A

STN - pod-shaped, located rostral and lateral to substantia nigra

Output is excitatory (Glutamatergic)

318
Q

What is the globus pallidus?

A

Located lateral to the interanl capsule and medial to the putamen

3 parts: External, internal, ventral

External (GPe) and inner (GPi) are dorsal pallidum; ventral pallidum (VP) is ventral to anterior commissure

All are GABAergic

319
Q

What is the substantia nigra?

A

Two parts (pars reticulata (SNpr), and pars compacta (SNpc))

SNpr is caudomedial extension of GPi = both are GABAergic

SNpc is midbrain dopaminergic cell group that provides input to striatal MSN

320
Q

Which are the major output centers of the basal ganglia?

A

GPi, SNpr and VP

321
Q

Which basal ganglia output center contorls head and neck motor control?

A

SNpr

322
Q

Which basal ganglia output center controls motor body function?

A

GPi

323
Q

How does output to the pyramidal system occur from the basal ganglia?

A

GPi/SNpr axons travel to thalamus via ansa lenticularis and lenticular fasciculus

324
Q

What are the important functions of the ansa lenticularis and lenticular fasciculus?

A

Tracts of output from the GPi/SNpr axons to the thalamus

325
Q

What are the pathologic hallmark of parkinson’s disease?

A

Lewy bodies

326
Q

What is a lewy body?

A

Pathologic hallmark for Parkinson’s Disease

Eosinophilic inclusion in neuron made of alpha synuclein and ubiquitin

Classically in Substantia Nigra, but also found elsewhere

327
Q

How is Parkinson’s diagnosed?

A

Clinically

Cardinal signs:

Bradykinesia, rigidity, tremor, postural instability

328
Q

What is the characteristic parkinson’s tremor?

A

3Hz, 3-5Hz, pill rolling

329
Q

How is Parkinson’s treated?

A

Symptomatically - no cure

Levodopa (precursor to dopamine that crosses BBB)

MAOI -B inhibitors - increases dopamine levels

COMT inhibitors - keep plasma levodopa levels high

Amantadine - antiviral agent that keeps endogenous dopamine levels high

Anticholinergics

Deep brain Stimulation

330
Q

What is Lewy Body Dementia?

A

Parkinsonism, dementia, fluctuations in arousal and attention, myoclonus, visual hallucinations

331
Q

What is progressive supranuclear palsy (PSP)?

A

Symmetric Parkinsonism

Early postural instability with falls

Typically onset after 70 years old, and no response to levodopa

332
Q

What is Cortical basal ganglionic degeneration?

A

Rare condition with onset in 60s or 70s with rapid course

Asymmetric, atremulous parkinsonism

Cortical involvement with issues writing, aphasia

no response to levodopa

333
Q

What is multiple system atrophy?

A

Onset in 40s-60s and can mimic Parkinson’s

parkinsonian, cerebellar, or autonomic

early autonomic dysfunction (orthostatic, incontinence)

symmetrical parkinsonism, with rapid progression

334
Q

What is Wilson’s Disease?

A

Movement disorders that present at 10-25 years old with liver disease

(liver + neuro/psych = wilsons)

Can lead to renal failure, retardation

Dysarthria, dystonia, tremor, parkinsonism, Kaiser Fleischer rings (copper in cornea),

Autosomal recessive caused by mutations in copper transporter ATPase. Causes copper accumulation

If under 50 with parkinsonism = test for Wilsons!

Treat with chelators!!!!

335
Q

What is Huntington’s Disease?

A

Chorea - starts as clumsiness/fidgetiness progresses to full chorea

Dysarthria, dysphagia, motor impersistence

Parkinsonism

Depression, psychosis, dementia

Slowed saccades

Atrophy of the striatum - particularly caudate

Initially degenerates indirect pathway, eventually both

Treat with Dopa antagonists and Dopa depleting agents

Autosomal dominant - CAG repeats in huntingtin gene (Chr 4 >38 repeats

336
Q

What is chorea?

A

Involuntary continual irregualr and unsustained movements

Not predicatable or suppresable

Motor impersistence, mild hypotonia

In Huntingtons, side effect of L-Dopa, antipsychotics

337
Q

What are tics?

A

Unvoluntary production of movements, sounds

Premonition sensation, suppressible, suggestible, stereotyped

Childhood onset, co-occurs with OCD, ADHD (Tourette’s)

338
Q

What are tremors?

A

Involuntary rhythmic oscillations, usually 3-12 Hz

Essentail tremor = head, hands voice (6Hz)

Cerebellar dysfunction = 3 Hz

Parkinsonism = 3Hz

Alcohol improves essential tremor

Treat with DBS, botulinum, anticonvulsants

339
Q

What is dystonia?

A

Slow, twisting, repetitive movements that produce abnormal postures

Task specific, persist over time, spread

Sensory tricks can aleviate

Dopamine, ACh dysfunction in basal ganglia

340
Q

What happens in hypokinesis?

A

Indirect pathway dominates over direct pathway - net inhibition of thalamus - decreased cortical output - decreased quality of movement

Parkinsons = loss of Dopaminergic SNpc neurons

341
Q

What happens in hyperkinesis?

A

Direct pathwya predominates over indirect pathway with net disinhibition of the thalamus - increased cortical signals - increased movement

Huntingtons - death of neurons that initiate indirect pathway; D1 Substance P MSNs are spared, but lost over time

Brain and Behavior (9 decks)

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