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
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
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
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
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
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
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
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
9
Q
Motor Strength: Weak Atrophy: Present Deep Tendon Reflexes: Hypoactive or absent Muscle Tone: Hypotonic (flaccid) Abnormal Movements: Fasciculations
A
Lower Motor Neuron
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
11
Q
Evaluation of the Motor System
A
History, Physical Examination, Neurologic Examination, Laboratory Work-up»_space;> LOCALIZATION; DIFFERENTIAL DIAGNOSIS
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
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
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
15
Q
defect in hyperthyroidism is abnormal deposition of fat sa
likod ng mata
A
EXOPHTHALMOS
16
Q
abnormal blood vessels seen in chronic alcoholic disease,
liver cirrhosis
A
SPIDER ANGIOMA
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)
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
19
Q
Grading: Reflexes
A
0 -no reflex \+1-hyporefflex \+2-normal \+3-hyperreflex \+4-abnormal reflexes (e.g. babinski)
20
Q
Etiologies of Lesion affecting Motor Tract
A
- Traumatic
- Neoplasmic
- Vascular
- Metabolic/Toxic
- Degenerative
- Congenital/Developmental
- Infectious
Immunologic
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
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)»_space;cortex affected
- Lesion: L frontal lobe
- Dx: Stroke
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)
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
25
- 35/ M
- L-sided weakness
- Frequent jerking of the L extremities
- Headache x 3 mos
- Vomiting
- Increased sleeping time
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)
26
- 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
```
Analysis:
FALCINE MENINGIOMA
- motor system
- upper motor neuron
- Lesion: Midline, left and right cortex (area also for control of urination)
```
27
```
- 65 / M with gradually progressive weakness of all
extremities
- Generalized atrophy and fasciculations
- Hyperrflexic all extremities
- Bilateral Babinski and clonus
- No sensory deficits
```
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
28
- Demyelinating disease
- Involves the cerebral hemispheres, brainstem, cranial nerves and spinal cord
- With remissions and exacerbations
MULTIPLE SCLEROSIS
29
```
- 65 / M with gradually progressive weakness of all
extremities
- Generalized atrophy and fasciculations
- Hyperrflexic all extremities
- Bilateral Babinski and clonus
- No sensory deficits
```
```
Analysis:
AMYOTROPHIC LATERAL SCLEROSIS
- motor system
- upper motor neuron (babinski and hyperreflexia); lower motor neuron (atrophy and fasciculations)
- Lesion: Anterior horn
```
30
- 3 month-old boy
- Born with lumbosacral mass
- Hypoplastic, flaccid bilateral LE
- Areflexic both LE
- Urinary incontinence
Analysis:
| LUMBAR MYELOMENINGOCELE
31
- 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)
LUMBAR MYELOMENINGOCELE
32
- 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
Analysis:
| GUILLAIN-BARRE SYNDROME
33
- 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
GUILLAIN-BARRE SYNDROME
34
- 22 / F with fluctuating bilateral extremity weakness
- Bilateral ptosis
- (+) dysphagia , dysarthria
- Symptoms worse at nighttime
- No sensory deficits
- Normal reflexes
- Enlarged thymus on CXray
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)
35
- 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
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
36
Motor Strength: Weak (Proximal
PERIPHERAL NERVE
37
```
Motor Strength: Weak (Proximal > Distal)
Atrophy: Present but may have pseudohypertophy
Deept Tendon Reflex: Hypoactive
Muscle Tone: Flaccid
Abnormal Movements: None
```
MUSCLE
38
3 Functional Divisions of the Cerebellum
1. Paleocerebellum
2. Neocerebellum
3. Archicerebellum
39
- 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.
Paleocerebellum
40
- 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.
Neocerebellum
41
- 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.
Archicerebellum
42
Internal Structure of the Cerebellum
Gray matter – outside and inside (Small aggregations of gray matter in the interior, called cerebellar nuclei)
White matter – inside
43
Gray matter of the Cerebellum: 3 layers
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
44
Gray matter of the Cerebellum:
- 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
45
Gray matter of the Cerebellum: 4 Intracerebellar Nuclei
1. Dentate
2. Emboliform
3. Globose
4. Fastigial
46
Cerebellar Output
1. Fastigial >> medial descending systems >> motor execution
2. Interposed >> lateral descending systems >> motor execution
3. Dentate >> areas 4 and 6 >> motor planning
4. vestibular nuclei >> balance and eye movement
47
White matter of the Cerebellum
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
48
Cerebellar Peduncles
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
49
Inferior Cerebellar Peduncle: Afferent Tracts
```
THE DORSAL SPINOCEREBELLAR TRACT
The cuneocerebellar tract
The olivocerebellar tract
THE VESTIBULOCEREBELLAR TRACT
The reticulocerebellar tract
The arcuatocerebellar tract
```
50
Inferior Cerebellar Peduncle: Efferent Tracts
Fastigiobulbar tract
| Cerebelloreticular tracts
51
Middle Cerebellar Peduncle
Afferent tracts - Fibers from the pontocerebellar tract (corticopontocerebellar tract)
52
Superior Cerebellar Peduncle: Afferent tracts
THE VENTRAL SPINOCEREBELLAR TRACT
The tectocerebellar tract
The trigeminocerebellar tract
The cerulocerebellar tract
53
Superior Cerebellar Peduncle: Efferent tracts
The dentatorubral tract
THE DENTATOTHALAMIC TRACT
The uncinate bundle of Russell
54
Clinical Features of Cerebellar Dysfunction
- Incoordination (ataxia) of volitional movement
- A characteristic tremor (“intention” or ataxic tremor)
- Disorders of equilibrium and gait
- Diminished muscle tone
55
- “Cerebellar sign par excellence”
| - May affect the limbs, trunk or gait
Ataxia or dystaxia
56
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
Asynergia
57
Abnormalities in the rate, range and force of movement
Dysmetria
58
abnormality in the rhythm of rapid alternating movements
Adiodochokinesis; Dysdiadochokinesis
59
- 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)
Hypotonia
60
- 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
Intention or ataxic tremor
61
- Scanning dysarthria
- Speech production is often labored with excessive facial grimacing.
- Thought to be a result of generalized hypotonia.
Cerebellar Dysarthria
62
variable intonation (prosody) and abnormalities in articulation; described also as staccato, explosive, hesitant, slow altered accent, and garbled speech.
Scanning dysarthria
63
A rhythmic tremor of the head or upper trunk (three to four per second)
Titubation
64
- overshooting the target; When the finger approaches the target, there is a side-to-side movement of the finger before reaching the target.
Hypermetria
65
Disturbances of Ocular Movement
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
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
Nystagmus
67
Disorders of Equilibrium and Gait
- 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
4 Cerebellar Syndrome
1. Hemispheric Syndrome
2. Rostral Vermis Syndrome
3. Caudal Vermis Syndrome
4. Pancerebellar Syndrome
69
- Incoordination of ipsilateral appendicular movements
| - *Usual etiologies: Infarcts, neoplasms, abscesses
Hemispheric syndrome
70
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
Rostral vermis syndrome
71
1. Axial disequilibrium (truncal ataxia) and staggering gait
2. Little or no limb ataxia
3. Sometimes spontaneous nystagmus and rotated postures of the head
Caudal vermis syndrome
72
- 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
```
Pancerebellar syndrome
73
Disorders of the Cerebellum
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
- 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
Cerebellar Strokes
75
Cerebellar Strokes
PICA 40%
AICA 5%
SCA 35%
Cortical watershed and deep cerebellar whitematter borderzone infarcts 20%
76
- Around 20% of metastases occur in the posterior fossa.
| - Usual neoplasms that metastasize to the brain parenchyma: lung, breast, melanoma, GI, kidney
Cerebellar Neoplasms
77
Primary Cerebellar Neoplasms
1. Medulloblastoma
2. Ependymoma and Papilloma of the 4th ventricle
3. Astrocytoma
4. Hemangioblastoma
78
- 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
Medulloblastoma
79
- 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
Ependymoma and Papilloma of the 4th ventricle
80
- May occur anywhere in the neuraxis
- Astrocytomas in the posterior fossa and optic nerves are more frequent in children and adolescents
- Juvenile pilocytic astrocytoma
Astrocytoma
81
- 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
Hemangioblastoma
82
- 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
Paraneoplastic Syndrome
83
- ~1/3 of cases, associated with small cell CA of the lung
- Ovarian CA – 25%
- Hodgkin lymphoma – 15%
- Breast, bowel, uterine CA
Paraneoplastic Cerebellar Degeneration
84
- 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
Paraneoplastic Syndromes involving the cerebellum
85
- 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
Brain Abscesses
86
- Behave as space-occupying lesions
| - Management depends on focus of infection and size of abscess
Cerebellar Abcess
87
- 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
Cerebellitis
88
- 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
Subdural empyema
89
Degenerative Diseases Involving the Cerebellum
1. Friedreich ataxia
2. Cerebellar atrophy
3. OPCA – olivopontocerebellar atrophy
90
- 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
Friedreich ataxia
91
- 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
Friedreich ataxia
92
- 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
Arnold-Chiari Syndrome
93
Clinical tests for arm dystaxia
- Ask the patient to extend the arms straight out front
- Do the finger to nose test
- Rapid pronation-supination test, thigh-slapping test
94
Clinical tests for leg dystaxia
- Heel-to-shin test
| - Heel-tapping test
95
Clinical tests for dystaxia of station and gait
- Observe the patient’s stance
- Ask the patient to walk
- Tandem-walk
96
Clinical demonstration of hypotonia
- Inspect for hypotonia – rag doll posture
- Checking for hypotonia
- Pendulous or hypotonic muscle stretch reflexes
97
Overshooting and checking tests of arms
- Wrist-slapping test
| - Arm-pulling test
98
Checking for Eye movements, speech
- Check smooth pursuit
| - Listen to patient’s speech
99
- 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
EXTRAPYRAMIDAL SYSTEM
100
EXTRAPYRAMIDAL SYSTEM: Function
Control and coordinate the postural, static, supporting and
| locomotor mechanism of movement
101
Extrapyramidal Tracts
- Rubrospinal tract
- Reticulospinal tract
- Olivospinal tract
- Vestibulospinal tract
- Tectospinal tract
102
- origin: red nucleus
- terminate at: anterior horn cell
- Decussates contralaterally
- Tract is located at lateral white matter.
- Function: Influence over flexor muscle tone
RUBROSPINAL TRACT
103
RUBROSPINAL TRACT
small bundle fibers arise from the NUCLEUS MAGNOCELLULARIS OF THE RED NUCLEUS >>
Cross to the opposite side (FOREL'S DECUSSATION) ventral to sylvian duct >>
Descend down through BRAINSTEM >>
enter the LATERAL WHITE COLUMN OF SPINAL CORD (anterior to corticospinal tract) >>
end at internuncial neuron at base of ANTERIOR HORN CELLS
104
RETICULOSPINAL TRACT
2 types of fibers: Both are Ipsilateral.
1. Medial Reticulospinal Fibers (MRF)
2. Lateral Reticulospinal Fibers (LRF)
105
Medial Reticulospinal Fibers (MRF) vs Lateral Reticulospinal Fibers (LRF)
Medial Reticulospinal Fibers (MRF) = PONTINE
origin: nuclei of reticularis pontis oralis
Lateral Reticulospinal Fibers (LRF) = MEDULLARY
Origin: Nucleus reticulo gigantocellularis
106
RETICULOSPINAL TRACT: FUNCTION
- 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
Medial Reticulospinal Fibers (MRF)
Pontine reticular formation from NUCLEI OF RETICULARIS PONTIS ORALIS AND CAUDALIS >>
IPSILATERALLY through longitudinal fasciculus >>
MEDIAL ASPECT OF ANTERIOR FUNICULUS >>
terminate gamma motor neurons at ANTERIOR GREY HORN IPSILATERALLY at all spinal level
108
Lateral Reticulospinal Fibers (LRF)
NUCLEUS RETICULARIS GIGANTOCELLULARIS in medulla >> some fibers cross, majority run IPSILATERALLY >> descend in ANTERIOR PART OF LATERAL FUNICULUS >>
terminate on GAMMA MOTOR NEURONS OF ANTERIOR HORN of spinal cord
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Point of Comparison: Pontine Reticular Fibers vs. Medullary Reticular Fibers
```
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
```
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- Origin: Superior Colliculus of Midbrain
- Functions:
* Control head movement (postural movement) in response to visual and auditory stimuli
* Decussates contralaterally
TECTOSPINAL TRACT
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TECTOSPINAL TRACT
SUPERIOR COLLICULUS OF MIDBRAIN >>
Cross in DORSAL TEGMENTAL DECUSSATION (DECUSSATION OF MEYNERY) >>
descend to ANTERIOR WHITE FUNICULUS OF SPINAL CORD >> terminate on ANTERIOR HORN CELLS OF SPINAL CORD
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VESTIBULOSPINAL TRACT: 2 Types of fibers
1. Medial Vestibulospinal Tract
| 2. Lateral Vestibulospinal Tract
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- 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
Medial Vestibulospinal Tract
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- 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
Lateral Vestibulospinal Tract
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Medial Vestibulospinal Tract
Medial vestibular nucleus in medulla >>
Bilateral but majority uncrossed into anterior white funiculus >>
terminate in neurons of anterior horn of spinal cord
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Lateral Vestibulospinal Tract
Lateral vestibular nucleus (DEITER'S NUCLEUS) in medulla>> descend UNCROSSED in anterior white funiculus >> terminate in ANTERIOR HORN OF SPINAL CORD
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- Also called Bulbospinal Tract / Tract of Helweg
- Origin: Medulla – Inferior Olivary nucleus
- Found in cervical region only!
- Functions: Facilitate reflex movement arising from proprioception
OLIVOSPINAL TRACT
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OLIVOSPINAL TRACT
arise from INFERIOR OLIVARY NUCLEUS >> enter the ANTERIOR PART OF THE LATERAL WHITE FUNICULUS of the spinal cord >> terminate in ANTERIOR HORN CELLS OF SPINAL CORD
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Structures that comprises the basal ganglia:
- Caudate
- Thalamus
- Lentiform Nuclei
* Putamen
* Globus Pallidus (Globus Pallidus Interna-GPi and Globus Pallidus Externa-GPe)
- Subthalamic Nuclei
- Substatntia Nigra
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2 fasciculi that connects thalamus and Globus Pallidus
| Interna (GPi)
1. Ansa Lenticularis
| 2. Lenticularis Fasciculus
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- pathway that conveys information from GPi to the motor
thalamus VA/VL
- loops under the posterior limb of internal capsule
- “jug handle
Ansa Lenticularis
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- Pathway that conveys information from GPi to the motor
thalamus
- Pass through the posterior limb of the internal capsule
Lenticularis fasciculus
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- combined bundle of the Ansa Lenticularis and Lenticular Fasciculus
Thalamic fasciculus
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Basal Ganglia: Pathway
all cortical areas involved in the planning and execution of movements project to the striatum (caudate and putamen)>>
striatal neurons project to GLOBUS PALLIDUS >>
Globus pallidus project to the THALAMUS VA/VL >>
Thalamus VA/VL project to the MOTOR CORTEX
* no descending pathway from basal ganglia direct to spinal cord
* will affect contralateral side
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Forms Lenticular nucleus
Globus Pallidus and Putamen
126
Forms Striatum
Caudate Nucleus and Putamen
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2 Pathways from the striatum to the GPi which have
| opposite effect on motor activity
1. Direct pathway
| 2. Indirect pathway
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- 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.
Direct pathway
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Direct pathway
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
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- 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
Indirect pathway
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Indirect pathway
GABA will inhibit STN = dec. stimulation of GPi = inc. production of GABA = inhibit thalamus = dec. in activity (slower movement, dec. firing rate)
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Direct vs Indirect Pathway
DIRECT PATHWAY turns UP motor activity
| INDIRECT PATHWAY turns DOWN motor activity
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The striatum is modulated by 2 important neuromedullary
| systems.
1. Dopaminergic
| 2. Cholinergic
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- 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
Dopaminergic
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- 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
Cholinergic neurons
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Movement Disorders
* Parkinsonism
* Chorea
* Hemiballism
* Athetosis
* Dystonia
* Tardive Dyskinesia
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Damage to the basal ganglia causes two different classes of syndromes:
1. Hyperkinetic – increase in movement
| 2. Hypokinetic – decrease in movement
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- 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.
PARKINSONISM
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- 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.
Chorea
140
- 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
Huntington’s Chorea
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- 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)
Hemiballismus
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- “snake-like movement”
- Involuntary, slow, twisting, writhing movements of
the trunks and limbs
- Striatal injury, particularly prominent in the PUTAMEN
Athetosis
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- 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
Dystonia
Neuroscience
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