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YL1: Neuroscience > Module 5 > Flashcards

Module 5 Flashcards

1
Q
  • Lack or diminution of muscle strength
  • Leads to inability to perform the usual function of a given
    muscle or group of muscles
  • “Fatigue” – subjective perception
  • Usually referable to a dysfunction of the corticospinal tract
  • Could be associated with gait disturbances or muscle
    atrophy but not all the time
A

Weakness

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2
Q

THE MOTOR PATHWAY

A 
Motor Cortex
Corona radiata
Internal capsule
Cerebral peduncle
Brainstem
Cervicomedullary junction
Corticospinal tract
Anterior horn cell
Ventral root
Peripheral nerve
Neuromuscular junction
Muscle
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3
Q
  • All the axons will radiate to corona radiata to gather into
    internal capsule then into cerebral peduncle down to
    midbrain, pons, medulla and then will decussate then
    descend to lateral corticospinal tract.
  • It descends to white matter of spinal cord then eventually
    to the gray into the ventral horn where the 1st neuron
    will synapse to the 2nd neuron.
  • Another axon will come out called the ventral root which
    is motor that joins the dorsal root which is sensory to form
    a single peripheral nerve.
  • Then goes to neuromuscular junction and to the muscle.
A

THE MOTOR PATHWAY

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4
Q
  • Can be found in frontal lobe 4-5mm top of brain.
  • Gray matter is gray because all the cell bodies are there.
  • White matter underneath contains all the axons that comes down as corona radiata.
A

THE MOTOR CORTEX

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5
Q
  • 1st cell body(neuron) in the cortex that goes to 2nd cell
    body(neuron) in the anterior horn then to the muscle.
  • Dalawa lang ang neurons na maeencounter. Yung 1st
    neuron, yun yung upper motor neuron, any lesions from
    cortex to spinal cord
  • Yung 2nd neuron yun yung lower motor neuron. Any
    lesions from spinal cord to muscles.
  • If above decussation, it will be contralateral. If below
    decussation, it will be ipsilateral.
A

THE PYRAMIDAL TRACT

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6
Q
  • If the command is to make your face smile, it will NOT
    continue the corticospinal tract that proceeds to spinal cord
    but will stop and proceed to corticobulbar tract.
  • Same lang sya sa starting point ng corticospinal path yun
    nga lang mas maaga nagstop. Then sa nucleus ng facial
    nerve sa pons, may axon na lalabas dun that will form the
    peripheral nerve. This is the counter part to the anterior horn in the spinal cord.
  • Cranial nerve is a peripheral nerve in the lower motor
    neuron (in the corticobulbar tract).
A

THE CORTICO BULBAR TRACT

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7
Q
  • Its nucleus receives inputs from contralateral and ipsilateral cortex, double innervations.
  • When you cut the contralateral tract like in stroke, it will
    affect the lower muscles but not the upper because of the
    innervations of the ipsilateral cortex.
  • Paralyzed ung kalahati pero pagpinapikit mo makakapikit pa rin siya.
A

Facial Nerve

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8
Q 
Motor Strength: Weak
Atrophy: Mild (Atrophy of disuse)
Deep Tendon Reflexes: Hyperactive
Muscle Tone: Hypertonic (spastic)
Abnormal Movements: Withdrawal spasms, abnormal reflexes
A

Upper Motor Neuron

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9
Q 
Motor Strength: Weak
Atrophy: Present
Deep Tendon Reflexes: Hypoactive or absent
Muscle Tone: Hypotonic (flaccid)
Abnormal Movements: Fasciculations
A

Lower Motor Neuron

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10
Q

affected ang lower motor neuron kasi hindi niya maclose
maigi yung isang eye at hindi niya masmile yung isang side
ng fac

A

Bell’s Palsy

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11
Q

Evaluation of the Motor System

A

History, Physical Examination, Neurologic Examination, Laboratory Work-up&raquo_space;> LOCALIZATION; DIFFERENTIAL DIAGNOSIS

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12
Q

History Taking

A

Onset : acute, chronic
Course : progressive, remissions and exacerbations
Distribution : proximal, distal, hemiparetic, paraplegic Associated neurologic symptoms : dysphagia,
dysarthria, diplopia, ataxia, numbness, paresthesias,
seizures
Others : fever, exposure to toxins, medications

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13
Q

Remember (History Taking)

A

*Progressive (increase ung line) - possible tumor
*Remission (wavy line) - multiple sclerosis
*Continuous (straight line) - congenital cause
*Proximal will be the trunk;
*Distal will be your fingers and your toes
*Hemiparesis/hemiplegia is not a zero weakness, It is either
right or left.
*Paraplegia/paraparesis is a level down,lesion in the spinal
cord

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14
Q

Remember (History Taking) 2

A
  • Dysphagia- difficulty swallowing
  • Dysarthria-slurring of speech
  • Diplopia- double of vision
  • Ataxia-loss of balance
  • Paresthesias- abnormal sensations
  • Seizures- arise from cortex
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15
Q

defect in hyperthyroidism is abnormal deposition of fat sa

likod ng mata

A

EXOPHTHALMOS

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16
Q

abnormal blood vessels seen in chronic alcoholic disease,

liver cirrhosis

A

SPIDER ANGIOMA

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17
Q

Neurologic Examination

A
  • Distribution of weakness
  • Muscle bulk
  • Muscle tone
  • Key muscles involved
  • Deep tendon reflexes
  • muscle bulk
  • look for atrophy
  • muscle tone
  • spastic (stroke)
  • rigid (parkinson’s)
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18
Q

Grading: Motor Strength

A 
0/5-no movement
1/5-flicker movement, twitch
2/5-side to side motion
3/5-can go against gravity
4/5-against minimal resistance
5/5-maximal resistance, pwedeng mag arm wrestling
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19
Q

Grading: Reflexes

A 
0 -no reflex
\+1-hyporefflex
\+2-normal
\+3-hyperreflex
\+4-abnormal reflexes (e.g. babinski)
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20
Q

Etiologies of Lesion affecting Motor Tract

A
  • Traumatic
  • Neoplasmic
  • Vascular
  • Metabolic/Toxic
  • Degenerative
  • Congenital/Developmental
  • Infectious
     Immunologic
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21
Q
  • 72/F with three month history of headache and left-sided
    weakness
  • Also had two episodes of focal seizures described as
    jerking of the left arm lasting for a few seconds
  • On PE, R 5/5, L 3/5
    DTR: ++/+++, Babinski L
    spastic L extremities
A 
Analysis:
motor system
UMN (spasticity, hyperreflexia, Babinski)
Seizure (cortex)
Lesion: R Frontal Cortex
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22
Q
  • 70/F known hypertensive and diabetic with no meds
  • 3 hours prior to admission
  • sudden onset of right-sided weakness, decrease in sensorium
  • BP = 150/100 HR = 90-100 (irregular)
  • Drowsy, aphasic
  • Hemianopsia R
  • Shallow R nasolabial fold
  • Tongue deviated to the R
  • Hemiplegia, right
  • DTRs : ++ L, +++ R
  • Babinski, R
A

Analysis:

  • motor system
  • upper motor neuron (hyperreflexia, babinski)
  • hemianopsia, drowsy, aphasic (affected ang Broca’s)&raquo_space;cortex affected
  • Lesion: L frontal lobe
  • Dx: Stroke
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23
Q 
- 22 / M gradually progressive right-sided weakness and
headache
- Aphasic
- R homonymous hemianopsia
- Motor strength R 2/5, L 4/5
- Spastic extemities R
- Hyperreflexia R
A

Analysis:
ARTERIOVENOUS MALFORMATION (abnormal blood vessel)
- Behave like a tumor. Pero bakit hindi considered as tumor?
- Kasi masyadong bata magkaroon ng tumor, unlike sa adult,tumor kaagad ang possible diagnosis.
- motor system
- upper motor neuron
- Lesion: L frontal (aphasic)

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24
Q

RULE of 7

A

7 hrs. maybe a stroke;
7 days maybe infectious;
7 months maybe a tumor;
7 years maybe congenital or degenerative

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25
Q
  • 35/ M
  • L-sided weakness
  • Frequent jerking of the L extremities
  • Headache x 3 mos
  • Vomiting
  • Increased sleeping time
A

Analysis:
GLIOBLASTOMA MULTIFORME
- additional assessments: motor strength 2/5 L, 5/5 R;
hyperreflexia and babinski on the left
- motor system
- upper motor neuron
- Lesion: R frontal lobe motor cortex (jerking-seizure)

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26
Q
  • 55/F with gradually progressive bilateral lower extremity
    weakness x 6 months
  • (+) incontinence, behavioral changes, headache
  • Focal seizures R leg with secondary generalization
  • Both LE spastic, hyperreflexic
A 
Analysis:
FALCINE MENINGIOMA
- motor system
- upper motor neuron
- Lesion: Midline, left and right cortex (area also for control of urination)
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27
Q 
- 65 / M with gradually progressive weakness of all
extremities
- Generalized atrophy and fasciculations
- Hyperrflexic all extremities
- Bilateral Babinski and clonus
- No sensory deficits
A

Analysis:
MULTIPLE SCLEROSIS
- immune system attacks the myelin sheath resulting to
multiple lesions
- treatment focuses on the control of immune system
 motor system
- may involve upper and lower motor neurons

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28
Q
  • Demyelinating disease
  • Involves the cerebral hemispheres, brainstem, cranial nerves and spinal cord
  • With remissions and exacerbations
A

MULTIPLE SCLEROSIS

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29
Q 
- 65 / M with gradually progressive weakness of all
extremities
- Generalized atrophy and fasciculations
- Hyperrflexic all extremities
- Bilateral Babinski and clonus
- No sensory deficits
A 
Analysis:
AMYOTROPHIC LATERAL SCLEROSIS
- motor system
- upper motor neuron (babinski and hyperreflexia); lower motor neuron (atrophy and fasciculations)
- Lesion: Anterior horn
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30
Q
  • 3 month-old boy
  • Born with lumbosacral mass
  • Hypoplastic, flaccid bilateral LE
  • Areflexic both LE
  • Urinary incontinence
A

Analysis:

LUMBAR MYELOMENINGOCELE

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31
Q
  • closure of vertebrae is incomplete, the lesion contains
    nerve roots, meninges and CSF
  • caused by taking medications, drinking alcohol and
    smoking during 1st 3 weeks of pregnancy
  • women should take folic acid 400 micrograms before
    getting pregnant
  • motor system
  • lower motor neuron (affects spinal cord)
A

LUMBAR MYELOMENINGOCELE

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32
Q
  • 14 / F with history of fever and cough x 2 weeks
  • Developed acute ascending lower extremity weakness
    and numbess
  • Arreflexic and flaccid all extremities
  • Hypoesthesia from waist down
A

Analysis:

GUILLAIN-BARRE SYNDROME

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33
Q
  • always preceded by viral infection (flu, cough, cold or
    diarrhea)
  • Kapag natapos nang labanan ng immune system mo
    yung virus, nagiging hyper siya kaya naghahanap pa
    siya ng kakalabanin. Nagkataon na kamukha ng virus
    yung myelin sheath ng peripheral nerve and starts to eat
    it. Now you will have a peripheral neuropathy.
  • lower motor neuron (from anterior horn to muscle)
  • peripheral nerve affected - ascending weakness and
    numbness
  • sa peripheral nerve ka lang nagkakaroon ng combined
    motor and sensory
A

GUILLAIN-BARRE SYNDROME

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34
Q
  • 22 / F with fluctuating bilateral extremity weakness
  • Bilateral ptosis
  • (+) dysphagia , dysarthria
  • Symptoms worse at nighttime
  • No sensory deficits
  • Normal reflexes
  • Enlarged thymus on CXray
A

Analysis:
MYASTHENIA GRAVIS
- motor system is not involved because all reflexes are
normal
- peripheral nerve is normal
- immune system eats up your AcH receptors.
- affected ang Neuromuscular Junction. Waxing and
wanning ang characteristic niya.
- in morning they’re superman, at night they’re lowbatt
- enlarged thymus (puno ng lymphocytes)

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35
Q
  • 8 year-old boy with difficulty of breathing
  • Started walking at 4 y.o.
  • (+) waddling gait
  • (+) Gower’s sign
  • Weak proximal muscles
  • Normal reflexes
  • Similar illness in maternal uncle
A

Analysis:
MUSCULAR DYSTROPHY (DUCHENNE’S)
- X-LINKED, seen in males
- Gower’s sign - when you stand from sitting, you use
your arms, then your knees and gradually go up. Sign of
proximal weakness.
- motor system is not involved because of normal reflexes
- pag proximal affected ang muscle, kapag distal nerve
ang affected

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36
Q

Motor Strength: Weak (Proximal

A

PERIPHERAL NERVE

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37
Q 
Motor Strength: Weak (Proximal > Distal)
Atrophy: Present but may have pseudohypertophy
Deept Tendon Reflex: Hypoactive
Muscle Tone: Flaccid
Abnormal Movements: None
A

MUSCLE

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38
Q

3 Functional Divisions of the Cerebellum

A
  1. Paleocerebellum
  2. Neocerebellum
  3. Archicerebellum
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39
Q
  • Consists of the vermis of the anterior lobe, the pyramids, the uvula, and the paraflocculus
  • Also known as the spinocerebellum
  • Plays a role in the control of muscle tone and the axial and limb movements.
A

Paleocerebellum

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40
Q
  • Corticocerebellum or cerebrocerebellum
  • Consists of the middle portion of the vermis and most of the cerebellar hemispheres
  • Also known as pontocerebellum
  • Projects fibers to the cerebral cortex through the thalamus
  • Plays a role in the planning and initiation of movements, as well as regulation of fine limb movements.
A

Neocerebellum

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41
Q
  • Corresponds to the flocculonodular lobe
  • Also called the vestibulocerebellum
  • Receives input from areas of the brain concerned with eye movements
  • Plays a role in the control of body equilibrium and eye movements.
A

Archicerebellum

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42
Q

Internal Structure of the Cerebellum

A

Gray matter – outside and inside (Small aggregations of gray matter in the interior, called cerebellar nuclei)

White matter – inside

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43
Q

Gray matter of the Cerebellum: 3 layers

A
  1. Molecular layer – stellate cells, basket cells
  2. Purkinje cell layer – Purkinje cells, which are large Golgi type 1 neurons
  3. Granular layer – granule cells (fibers of which form parallel fibers), neuroglial cells, Golgi cells
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44
Q

Gray matter of the Cerebellum:

A
  • Purkinje cell – output
  • Mainly inhibitory except granule cells (utilizes glutamate)
  • Main neurotransmitter: γ-ABA
  • Output of the cerebellar nuclei is excitatory but is modulated by an inhibitory cortical loop, effected by Purkinje Cell output
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45
Q

Gray matter of the Cerebellum: 4 Intracerebellar Nuclei

A
  1. Dentate
  2. Emboliform
  3. Globose
  4. Fastigial
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46
Q

Cerebellar Output

A
  1. Fastigial&raquo_space; medial descending systems&raquo_space; motor execution
  2. Interposed&raquo_space; lateral descending systems&raquo_space; motor execution
  3. Dentate&raquo_space; areas 4 and 6&raquo_space; motor planning
  4. vestibular nuclei&raquo_space; balance and eye movement
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47
Q

White matter of the Cerebellum

A
  1. Intrinsic fibers – connect different regions WITHIN the cerebellum (folium-folium; hemisphere-hemisphere)
  2. Afferent fibers – form the greater part of the white matter, PROCEED to the cerebellar cortex; enter though the INFERIOR and MIDDLE cerebellar peduncles
    3 types: mossy (predominantly), climbing (olivocerebellar tracts), multilayered
  3. Efferent fibers – constitute the OUTPUT of the cerebellum; commence as the axons of the Purkinje cells, which synapse with the neurons of the cerebellar nuclei; exit mainly through the SUPERIOR and INFERIOR cerebellar peduncle
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48
Q

Cerebellar Peduncles

A
  1. Inferior Cerebellar Peduncle – connects to the medulla oblongata; restiform body
  2. Middle Cerebellar Peduncle – connects to the pons; brachium pontis
  3. Superior Cerebellar Peduncle – connects to the midbrain; brachium conjunctivum
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49
Q

Inferior Cerebellar Peduncle: Afferent Tracts

A 
THE DORSAL SPINOCEREBELLAR TRACT
The cuneocerebellar tract
The olivocerebellar tract
THE VESTIBULOCEREBELLAR TRACT
The reticulocerebellar tract
The arcuatocerebellar tract
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50
Q

Inferior Cerebellar Peduncle: Efferent Tracts

A

Fastigiobulbar tract

Cerebelloreticular tracts

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51
Q

Middle Cerebellar Peduncle

A

Afferent tracts - Fibers from the pontocerebellar tract (corticopontocerebellar tract)

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52
Q

Superior Cerebellar Peduncle: Afferent tracts

A

THE VENTRAL SPINOCEREBELLAR TRACT
The tectocerebellar tract
The trigeminocerebellar tract
The cerulocerebellar tract

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53
Q

Superior Cerebellar Peduncle: Efferent tracts

A

The dentatorubral tract
THE DENTATOTHALAMIC TRACT
The uncinate bundle of Russell

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54
Q

Clinical Features of Cerebellar Dysfunction

A
  • Incoordination (ataxia) of volitional movement
  • A characteristic tremor (“intention” or ataxic tremor)
  • Disorders of equilibrium and gait
  • Diminished muscle tone
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55
Q
  • “Cerebellar sign par excellence”

- May affect the limbs, trunk or gait

A

Ataxia or dystaxia

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56
Q

lack of synergy of the various muscle components in performing more complex movements so that movements are disjointed and clumsy and broken up into isolated successive parts

A

Asynergia

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57
Q

Abnormalities in the rate, range and force of movement

A

Dysmetria

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58
Q

abnormality in the rhythm of rapid alternating movements

A

Adiodochokinesis; Dysdiadochokinesis

59
Q
  • It is related to a depression of gamma and alpha motor neuron activity
  • The least evident of the cerebellar abnormalities
  • More apparent with acute than with chronic lesions
  • Failure to check a movement - a closely related phenomenon (impairment of the check reflex)
A

Hypotonia

60
Q
  • Hypermetria – overshooting the target
    When the finger approaches the target, there is a side-to-side movement of the finger before reaching the target.
  • Titubation
A

Intention or ataxic tremor

61
Q
  • Scanning dysarthria
  • Speech production is often labored with excessive facial grimacing.
  • Thought to be a result of generalized hypotonia.
A

Cerebellar Dysarthria

62
Q

variable intonation (prosody) and abnormalities in articulation; described also as staccato, explosive, hesitant, slow altered accent, and garbled speech.

A

Scanning dysarthria

63
Q

A rhythmic tremor of the head or upper trunk (three to four per second)

A

Titubation

64
Q
  • overshooting the target; When the finger approaches the target, there is a side-to-side movement of the finger before reaching the target.
A

Hypermetria

65
Q

Disturbances of Ocular Movement

A
  1. Inability to hold eccentric gaze
  2. Slower smooth pursuit movements with “catch-up” saccades
  3. Nystagmus
  4. Other “cerebellar” eye signs – ocular flutter, opsoclonus, ocular bobbing, square wave jerks at rest, skew deviation, failure to suppress the vestibulo-ocular reflex
66
Q

usually gaze-evoked, upbeat, rebound with abnormal kinetic nystagmus if with midline cerebellar lesions; periodic alternating nystagmus with lesions of the uvula, nodulus; downbeat nystagmus with posterior midline lesions

A

Nystagmus

67
Q

Disorders of Equilibrium and Gait

A
  • Standing with feet together may be impossible
  • In walking, the patient’s steps may be uneven and placement of the foot may be misaligned
  • Wide-based stance with increased trunk sway, irregular stepping with a tendency to stagger as if intoxicated
  • Impaired tandem walking
68
Q

4 Cerebellar Syndrome

A
  1. Hemispheric Syndrome
  2. Rostral Vermis Syndrome
  3. Caudal Vermis Syndrome
  4. Pancerebellar Syndrome
69
Q
  • Incoordination of ipsilateral appendicular movements

- *Usual etiologies: Infarcts, neoplasms, abscesses

A

Hemispheric syndrome

70
Q
  1. A wide-based stance and titubating gait
  2. Ataxia of gait, with proportionally little ataxia on the heel-to-shin maneuver with the patient lying down
  3. Normal or only slightly impaired arm coordination
  4. Infrequent presence of hypotonia, nystagmus, and dysarthria
A

Rostral vermis syndrome

71
Q
  1. Axial disequilibrium (truncal ataxia) and staggering gait
  2. Little or no limb ataxia
  3. Sometimes spontaneous nystagmus and rotated postures of the head
A

Caudal vermis syndrome

72
Q
  • Bilateral signs of cerebellar dysfunction affecting the trunk, limbs, and cranial musculature
- Some etiologies:
infectious and parainfectious processes
hypoglycemia
hyperthermia
paraneoplastic cerebellar degeneration associated with small cell lung cancer (anti-Hu antibodies), breast and ovarian carcinomas (anti-Yo antibodies), or Hodgkin's lymphoma (Tr antibodies)
Toxic processes
A

Pancerebellar syndrome

73
Q

Disorders of the Cerebellum

A

V – Vascular – strokes, vasculitis
I – Infectious – cerebellitis, post-infectious conditions, abscesses
T – Traumatic, Toxic – gross trauma, drug toxicity
A – Autoimmune - paraneoplastic
M – Metabolic
I – Inflammatory
N – Neoplastic, Nutritional – alcoholism, paraneoplastic
D – Degenerative, Developmental (including Congenital), Demyelinating – Multiple sclerosis, spinocerebellar degeneration, Chiari malformations

74
Q
  • Symptoms: vertigo, dizziness, nausea, vomiting, gait unsteadiness, limb clumsiness, headache, dysarthria, diplopia and decreased level of alertness
  • Prominent signs: limb and gait ataxia, dysarthria, nystagmus, altered mental status
A

Cerebellar Strokes

75
Q

Cerebellar Strokes

A

PICA 40%
AICA 5%
SCA 35%
Cortical watershed and deep cerebellar whitematter borderzone infarcts 20%

76
Q
  • Around 20% of metastases occur in the posterior fossa.

- Usual neoplasms that metastasize to the brain parenchyma: lung, breast, melanoma, GI, kidney

A

Cerebellar Neoplasms

77
Q

Primary Cerebellar Neoplasms

A
  1. Medulloblastoma
  2. Ependymoma and Papilloma of the 4th ventricle
  3. Astrocytoma
  4. Hemangioblastoma
78
Q
  • Arises in the posterior part of the vermis and neuroepithelial roof of the fourth ventricle
  • ~20% (-25%) of childhood brain tumors
  • Occur in children around 4-8 years of age
  • Males> females
  • ~85% arise from the vermis
  • Usually hyperdense on non-contrast CT
  • Treatment: Maximal safe resection, treatment of hydrocephalus, craniospinal radiation, chemotherapy
A

Medulloblastoma

79
Q
  • Arises from the lining in the walls of the ventricles
  • ~70% originate from the 4th ventricle
  • Ependymomas are the third most common tumor in children
  • Choroid plexus tumors more common in children than adults
  • Ependymomas – may be cystic, may have signs of prior hemorrhaging, minimally to intensively enhances on contrast
  • Choroid plexus papillomas – may show calcification, intensively enhances
  • Treatment: address hydrocephalus, surgical resection; ? Chemotherapy for ependymomas, indicated if choroid plexus tumor is a carcinoma
A

Ependymoma and Papilloma of the 4th ventricle

80
Q
  • May occur anywhere in the neuraxis
  • Astrocytomas in the posterior fossa and optic nerves are more frequent in children and adolescents
  • Juvenile pilocytic astrocytoma
A

Astrocytoma

81
Q
  • Occur most often in association with von Hippel-Lindau disease (~25%; 50% of retinal tumors)
  • May have an associated retinal angioma, or hepatic and pancreatic cysts
  • Tendency to develop malignant renal or adrenal tumors
  • Pxs may have polycythemia due to elaboration of erythropoietic factor
A

Hemangioblastoma

82
Q
  • A neurologic disorder in patients with neoplasia even though the nervous system is not the site of the primary tumor, metastases nor its direct invasion
  • May predate the diagnosis of the primary carcinoma
  • Small cell cancer of the lung, adenocarcinoma of the breast and ovary, Hodgkin disease
  • Possibly autoimmune
A

Paraneoplastic Syndrome

83
Q
  • ~1/3 of cases, associated with small cell CA of the lung
  • Ovarian CA – 25%
  • Hodgkin lymphoma – 15%
  • Breast, bowel, uterine CA
A

Paraneoplastic Cerebellar Degeneration

84
Q
  • Subacute onset, with steady progression
  • Symmetric ataxia, nystagmus, dysarthria
  • Occasionally opsoclonus and myoclonus
  • Diplopia, vertigo, Babinski signs, ocular motility problems, sensorineural hearing loss, alteration of mentation and affect
  • Anti-Yo and anti-Hu antibodies
A

Paraneoplastic Syndromes involving the cerebellum

85
Q
  • Almost always secondary to a purulent focus elsewhere in the body
  • ~40% are related to diseases of the paranasal sinuses, middle ear, mastoid cells; 33% from distant foci
  • From otogenic sources, around 1/3 lie in the anterolateral part of the cerebellar hemisphere; the remainder occur in the middle and inferior parts of the temporal lobe
A

Brain Abscesses

86
Q
  • Behave as space-occupying lesions

- Management depends on focus of infection and size of abscess

A

Cerebellar Abcess

87
Q
  • Acute cerebellitis of childhood
  • Measles, pertussis and scarlet fever
  • Most often with chicken pox
  • Enteroviruses (Coxsackie), EBV, Mycoplasma, CMV, Q fever
  • EBV and Mycoplasma in adults
  • Infectious vs. post-infectious pathogenetic mechanisms
A

Cerebellitis

88
Q
  • Not as frequent as cerebral abscesses
  • Either by direct extension or hematogenously spread
  • From sinuses, mastoid cells
  • In the posterior fossa, occasionally found covering the cerebellum
A

Subdural empyema

89
Q

Degenerative Diseases Involving the Cerebellum

A
  1. Friedreich ataxia
  2. Cerebellar atrophy
  3. OPCA – olivopontocerebellar atrophy
90
Q
  • Accounts for half of all cases of progressive spinocerebellar ataxia
  • Onset in childhood
  • Within 5 years of onset, walking is no longer possible
  • Chromosome 9q13-2
A

Friedreich ataxia

91
Q
  • Ataxia of gait is the initial symptom – both sensory and cerebellar
  • Pes cavus and kyphoscoliosis precede the ataxia
  • Cardiomyopathy
  • Important causes of death are respiratory failure, cardiac arrhythmia, congestive heart failure
A

Friedreich ataxia

92
Q
  • Congenital anomalies at the base of the brain, consisting of:
    1. Extension of a tongue of cerebellar tissue into the cervical canal
    2. Displacement of the medulla into the cervical canal
  • Chiari II- associated with a meningomyelocoele
  • Hydomyelia, syringomyelia are common associated findings
A

Arnold-Chiari Syndrome

93
Q

Clinical tests for arm dystaxia

A
  • Ask the patient to extend the arms straight out front
  • Do the finger to nose test
  • Rapid pronation-supination test, thigh-slapping test
94
Q

Clinical tests for leg dystaxia

A
  • Heel-to-shin test

- Heel-tapping test

95
Q

Clinical tests for dystaxia of station and gait

A
  • Observe the patient’s stance
  • Ask the patient to walk
  • Tandem-walk
96
Q

Clinical demonstration of hypotonia

A
  • Inspect for hypotonia – rag doll posture
  • Checking for hypotonia
  • Pendulous or hypotonic muscle stretch reflexes
97
Q

Overshooting and checking tests of arms

A
  • Wrist-slapping test

- Arm-pulling test

98
Q

Checking for Eye movements, speech

A
  • Check smooth pursuit

- Listen to patient’s speech

99
Q
  • Any of the various brain structures affecting body movement that does not pass pyramidal tract
  • Functional rather than anatomical system
  • Compromised of nuclei and fibers (except pyramidal tract); involved in motor activities
A

EXTRAPYRAMIDAL SYSTEM

100
Q

EXTRAPYRAMIDAL SYSTEM: Function

A

Control and coordinate the postural, static, supporting and

locomotor mechanism of movement

101
Q

Extrapyramidal Tracts

A
  • Rubrospinal tract
  • Reticulospinal tract
  • Olivospinal tract
  • Vestibulospinal tract
  • Tectospinal tract
102
Q
  • origin: red nucleus
  • terminate at: anterior horn cell
  • Decussates contralaterally
  • Tract is located at lateral white matter.
  • Function: Influence over flexor muscle tone
A

RUBROSPINAL TRACT

103
Q

RUBROSPINAL TRACT

A

small bundle fibers arise from the NUCLEUS MAGNOCELLULARIS OF THE RED NUCLEUS&raquo_space;
Cross to the opposite side (FOREL’S DECUSSATION) ventral to sylvian duct&raquo_space;
Descend down through BRAINSTEM&raquo_space;
enter the LATERAL WHITE COLUMN OF SPINAL CORD (anterior to corticospinal tract)&raquo_space;
end at internuncial neuron at base of ANTERIOR HORN CELLS

104
Q

RETICULOSPINAL TRACT

A

2 types of fibers: Both are Ipsilateral.

  1. Medial Reticulospinal Fibers (MRF)
  2. Lateral Reticulospinal Fibers (LRF)
105
Q

Medial Reticulospinal Fibers (MRF) vs Lateral Reticulospinal Fibers (LRF)

A

Medial Reticulospinal Fibers (MRF) = PONTINE
origin: nuclei of reticularis pontis oralis

Lateral Reticulospinal Fibers (LRF) = MEDULLARY
Origin: Nucleus reticulo gigantocellularis

106
Q

RETICULOSPINAL TRACT: FUNCTION

A
  • Integrates information from the motor systems to coordinate automatic movements of locomotion and posture
  • Facilitates and inhibit involuntary movement, influences
    muscle tone
  • Mediates autonomic functions
  • Modulates pain impulses
  • Influences blood flow to the lateral geniculate
107
Q

Medial Reticulospinal Fibers (MRF)

A

Pontine reticular formation from NUCLEI OF RETICULARIS PONTIS ORALIS AND CAUDALIS&raquo_space;
IPSILATERALLY through longitudinal fasciculus&raquo_space;
MEDIAL ASPECT OF ANTERIOR FUNICULUS&raquo_space;
terminate gamma motor neurons at ANTERIOR GREY HORN IPSILATERALLY at all spinal level

108
Q

Lateral Reticulospinal Fibers (LRF)

A

NUCLEUS RETICULARIS GIGANTOCELLULARIS in medulla&raquo_space; some fibers cross, majority run IPSILATERALLY&raquo_space; descend in ANTERIOR PART OF LATERAL FUNICULUS&raquo_space;
terminate on GAMMA MOTOR NEURONS OF ANTERIOR HORN of spinal cord

109
Q

Point of Comparison: Pontine Reticular Fibers vs. Medullary Reticular Fibers

A 
Pontine Reticular Fibers
Voluntary and Reflex Movement: FACILITATE
Control of muscle tone: FACILITATE
Respiration: favor EXPIRATION
Blood Vessels: VASOCONSTRICTION
Medullary Reticular Fibers
Voluntary and Reflex Movement: INHIBITS
Control of muscle tone: INHIBITS
Respiration: favor INSPIRATION
Blood Vessels: VASODILATION
110
Q
  • Origin: Superior Colliculus of Midbrain
  • Functions:
  • Control head movement (postural movement) in response to visual and auditory stimuli
  • Decussates contralaterally
A

TECTOSPINAL TRACT

111
Q

TECTOSPINAL TRACT

A

SUPERIOR COLLICULUS OF MIDBRAIN&raquo_space;
Cross in DORSAL TEGMENTAL DECUSSATION (DECUSSATION OF MEYNERY)&raquo_space;
descend to ANTERIOR WHITE FUNICULUS OF SPINAL CORD&raquo_space; terminate on ANTERIOR HORN CELLS OF SPINAL CORD

112
Q

VESTIBULOSPINAL TRACT: 2 Types of fibers

A
  1. Medial Vestibulospinal Tract

2. Lateral Vestibulospinal Tract

113
Q
  • Origin: Medial vestibular nuclei
  • Terminate: Thoracic segment only
    -Functions
    *Concerned with adjustment of head and body during angular and linear acceleration
    *Concerned with conjugate horizontal eye movement,
    integration of eye and neck movements
A

Medial Vestibulospinal Tract

114
Q
  • Origin: Dieter’s nucleus
  • Tract descends throughout the spinal cord length
  • Functions
    *Facilitative influence on reflex spinal activities and spinal
    mechanism underlying muscle tone
    *Influences proximal limb muscles
A

Lateral Vestibulospinal Tract

115
Q

Medial Vestibulospinal Tract

A

Medial vestibular nucleus in medulla&raquo_space;
Bilateral but majority uncrossed into anterior white funiculus&raquo_space;
terminate in neurons of anterior horn of spinal cord

116
Q

Lateral Vestibulospinal Tract

A

Lateral vestibular nucleus (DEITER’S NUCLEUS) in medulla» descend UNCROSSED in anterior white funiculus&raquo_space; terminate in ANTERIOR HORN OF SPINAL CORD

117
Q
  • Also called Bulbospinal Tract / Tract of Helweg
  • Origin: Medulla – Inferior Olivary nucleus
  • Found in cervical region only!
  • Functions: Facilitate reflex movement arising from proprioception
A

OLIVOSPINAL TRACT

118
Q

OLIVOSPINAL TRACT

A

arise from INFERIOR OLIVARY NUCLEUS&raquo_space; enter the ANTERIOR PART OF THE LATERAL WHITE FUNICULUS of the spinal cord&raquo_space; terminate in ANTERIOR HORN CELLS OF SPINAL CORD

119
Q

Structures that comprises the basal ganglia:

A
  • Caudate
  • Thalamus
  • Lentiform Nuclei
  • Putamen
  • Globus Pallidus (Globus Pallidus Interna-GPi and Globus Pallidus Externa-GPe)
  • Subthalamic Nuclei
  • Substatntia Nigra
120
Q

2 fasciculi that connects thalamus and Globus Pallidus

Interna (GPi)

A
  1. Ansa Lenticularis

2. Lenticularis Fasciculus

121
Q
  • pathway that conveys information from GPi to the motor
    thalamus VA/VL
  • loops under the posterior limb of internal capsule
  • “jug handle
A

Ansa Lenticularis

122
Q
  • Pathway that conveys information from GPi to the motor
    thalamus
  • Pass through the posterior limb of the internal capsule
A

Lenticularis fasciculus

123
Q
  • combined bundle of the Ansa Lenticularis and Lenticular Fasciculus
A

Thalamic fasciculus

124
Q

Basal Ganglia: Pathway

A

all cortical areas involved in the planning and execution of movements project to the striatum (caudate and putamen)»
striatal neurons project to GLOBUS PALLIDUS&raquo_space;
Globus pallidus project to the THALAMUS VA/VL&raquo_space;
Thalamus VA/VL project to the MOTOR CORTEX

  • no descending pathway from basal ganglia direct to spinal cord
  • will affect contralateral side
125
Q

Forms Lenticular nucleus

A

Globus Pallidus and Putamen

126
Q

Forms Striatum

A

Caudate Nucleus and Putamen

127
Q

2 Pathways from the striatum to the GPi which have

opposite effect on motor activity

A
  1. Direct pathway

2. Indirect pathway

128
Q
  • The striatum project directly to GPi.
  • This pathway is to increase the excitatory drive from
    thalamus to cortex.
  • Cortical projection to the striatum use the excitatory
    transmitter glutamate to activate the striatum
  • Striatal cells use the inhibitory transmitter GABA to inhibit
    GPi.
  • GPi also uses GABA to inhibit the thalamus.
  • Thus, cortical signal excites striatal neurons, which result in MORE inhibition from the striatum to GPi. More inhibition of GPi means LESS inhibition of thalamus. VA/VL will
    INCREASE their firing and in turn the motor cortex.
     turns the motor system UP.
  • Cells in the VA/VL and motor cortex INCREASE their firing.
  • This results increased activity in the corticospinal tract and
    eventually the muscles.
A

Direct pathway

129
Q

Direct pathway

A

Cortex —(glutamate)—> Striatum —(GABA)—> GPi
—(GABA)—> Thalamus —(glutamate)—> Motor Cortex

  • glutamate= excitatory
  • GABA = inhibitory
  • 2 excitatory, 2 inhibitory
  • if you inhibit the inhibitory = you excite = DISINHIBITION
130
Q
  • Striatal neurons project to the Globus Pallidus externa.
    (GPe).
  • GPe now project to the subthalamic nuclei then to the GPi.
  • Turns DOWN the motor thalamus and in turn, motor cortex.
  • Thus, it turns down motor activity.
- Neurotransmitters
o Glutamate - excitatory
Projection neurons in the cortex
Subthalamic nucleus
VA / VL thalamus

o GABA – inhibitory
Both Globus Pallidus
Striatum

A

Indirect pathway

131
Q

Indirect pathway

A

GABA will inhibit STN = dec. stimulation of GPi = inc. production of GABA = inhibit thalamus = dec. in activity (slower movement, dec. firing rate)

132
Q

Direct vs Indirect Pathway

A

DIRECT PATHWAY turns UP motor activity

INDIRECT PATHWAY turns DOWN motor activity

133
Q

The striatum is modulated by 2 important neuromedullary

systems.

A
  1. Dopaminergic

2. Cholinergic

134
Q
  • Produced in Substantia Nigra specifically at pars compacta
  • Nigrostriatal axon terminals release dopamine into the
    striatum.
  • Both excitatory (direct pathway= D1) and inhibitory
    (indirect pathway = D2 receptor)
  • Increase motor activity
A

Dopaminergic

135
Q
  • There is a population of cholinergic neuron in the striatum
    whose axons do not leave the striatum (interneurons).
  • Action: inhibit striatal cell of direct pathway and excite
    the striatal cells of the indirect pathway
  • Net effect of Cholinergic Striatal Interneurons: decreased
    motor activity
A

Cholinergic neurons

136
Q

Movement Disorders

A
  • Parkinsonism
  • Chorea
  • Hemiballism
  • Athetosis
  • Dystonia
  • Tardive Dyskinesia
137
Q

Damage to the basal ganglia causes two different classes of syndromes:

A
  1. Hyperkinetic – increase in movement

2. Hypokinetic – decrease in movement

138
Q
  • Pathology: Dopaminergic neurons in Substantia Nigra Pars Compacta are lost.
  • Decrease in Dopamine = Direct Pathway
  • Compacta = decrease in direct pathway = excitation is lost
  • Ache neurons will not have inhibition
  • Characterized by rigidity, Bradykinesia, tremors and postural deficits.

Manifestations:

  • Rigidity and trembling of head
  • Forward tilt of trunk
  • Reduced arm swinging
  • Rigidity and trembling of extremities
  • Shuffling gait with short steps.
A

PARKINSONISM

139
Q
  • Characterized by involuntary choreiform movements which show up as rapid, involuntary, and purposeless jerks of irregular and variable location on the body.
  • They are spontaneous and cannot be inhibited, controlled or directed by the patient.
A

Chorea

140
Q
  • Pathology: Loss of GABA-ergic cells in the striatum that
    project only to GP external, the head of the indirect pathway.
  • Shows up on MRI as degeneration of the caudate
    nucleus.
  • Striatal cholinergic cells also begin to die.
  • Loss of both types of cells causes less inhibition of
    the VA/VL and increased motor output.
  • Lesion at caudate nucleus
  • Affects indirect pathway
  • Decrease cholinergic cells
A

Huntington’s Chorea

141
Q
  • Wild, flinging movements of the body due to a lesion in the subthalamic nucleus.
  • The excitatory input to GPi is lost, thus less inhibition reaching the VA/VL (STN normally increases the inhibition in the pallidal – VA/VL projection).
  • VA/VL is turned up, as is the motor cortex, and
    there is uncontrollable hyperactivity of the motor
    system.
  • Lesion at STN (which produces glutamate, which
    excited GPi)
A

Hemiballismus

142
Q
  • “snake-like movement”
  • Involuntary, slow, twisting, writhing movements of
    the trunks and limbs
  • Striatal injury, particularly prominent in the PUTAMEN
A

Athetosis

143
Q
  • Characterized by torsion spasms of the limbs, trunks and
    neck
  • Progressive or static but are usually idiopathic
  • Spasmodic torticollis is the most common idiopathic form
    characterized by intermittent excessive and involuntary
    contractions of the sternocleidomastoid muscle
A

Dystonia

YL1: Neuroscience (9 decks)

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