Upper and lower motor neurons Flashcards
Anterior horn ->nerve-> muscle
LMN
Brain-> Spine
UMN
Spastic
UMN
Hypertonic
UMN
Disuse Atrophy
UMN
+ Banbinski
UMN
Flaccid
LMN
Hypertonic
LMN
Hyporeflexic
LMN
Denervation Atrophy
LMN
-Babinski
LMN
Muscle is in spasm
Spastic
Muscles is limp/relax
Flaccid
We our not able to use the muscle due to injury
Disuse Atrophy
Lose innervation on the muscle
Denervation Atrophy
use reflex hammer stroke bottom of the foot, the toes curls down
- Banbinski
use reflex hammer stroke bottom of the foot, the toes curls up
+ Banbinski
clasp knife phenomenon
tighter in the middle range if motion then as we go towards end of range, that releases.
no rigidity of tremor
Spastisity
restruction of wrist movent ROM. tension in extending finger
UMN
Velocity dependent
UMN
Most affected in anti-gravity muscles
Biceps, Quads (hip flex), Hip
involuntary muscle contractions. 5-7hz contraction.
dorsiflex and plantarflex nakikita
Clonus
brisk reflexes
Hyperreflexia of deep tendon reflex
tapping the supratellar tendon will elicit knee jerk reflex
Hyperreflexia of deep tendon reflex
Superficial abdominal reflex and cremasterix reflex are decreased.
Hyporreflexia of superficial reflex
UMN
involuntary movements in a limb that have asscoiation to voluntary movements
Synkinesia
UMN
CN 7&12, WIP
Psuedo bulbar palsy
UMN
lumiliit muscles due to lack of nutrients
Muscle Atrophy
LMN
Weekness
LMN
Fasciculation
LMN
Damaged alpha motor neurons can produce spontaneous action potentials. These spikes cause the muscle fibers that are part of that neuron’s motor unit to fire, resulting in a visible twitch (called a ___) of the affected muscle.
Fasciculation
Fibrillation
LMN
Maliit na twicth
Fibrillation
Because alpha motor neurons are the only way to stimulate extrafusal muscle fibers, the loss of these neurons causes a decrease in muscle tone.
May strenght but less tone
Hypotonia
Hyporeflexia
LMN
D
The myotatic (stretch) reflex is weak or absent with lower motor neuron disorders, because the alpha motor neurons that cause muscle contraction are damaged.
Hyporeflexia
Weakness agad makikita
LMN
Late mainly because of disuse wasting
UMN
Early and present wasting
LMN
is the sudden occurrence of permanent damage to an area of the brain caused by a blocked blood vessel or bleeding within the brain. Other causes of focal brain damage, such as traumatic injury to the brain, demyelinating lesions, brain tumors, brain abscesses, and others, can produce stroke like symptoms but are not included in this definition.
Cerebrovascular Accident
Most common weakness of stroke
Focal weakness
Close head injury but Skull is not actually penetrated
Traumatic Brain Injury
Components of GCS
Eyes
Verbal
Motor
Abnormal flex/ abnormal slow flec. What is it and grade
Dicorticate, 3
complex, multifactorial disease that requires the expertise of neurologists, physiatrists, occupational therapists, and physical therapists, as well as countless other participants in the patient’s care.
Multiple Sclerosis
is considered to be an autoimmune diseases. Like all autoimmune disorders, it is more common in women, occurring about twice as often in women as in men. ➡
Multiple Sclerosis
also appears to involve genetic factors with HLA-DR2 in DR-positive families having a greater chance of developing the disease.
Multiple Sclerosis
The hallmark of MS pathology
Cardinal Symptoms:
Scanning Speech. Intention Tremor, Nystagmus also known as Charcot’s Triad.
The hallmark of MS pathology
Cardinal Symptoms:
Scanning Speech. Intention Tremor, Nystagmus also known as Charcot’s Triad.
Refers slowness of movement
Bradykinesia
Sx: Bradykinesia
Parkinson’s disease
Cardinal features of PD
Rigidity
o Bradykinesia
o Tremor
o Postural instability
Shaking palsy
Parkinson’s disease
Resistance of mm to passive elongation or stretch
Muscle tone
Tone is influenced
physical inertia
intrinsic mechanical-elastic stiffness of muscle and connective fissues.
spinal reflex muscle contraction (tonic strotch reflexos),
Hypertonic state characterized by constat resistance thoughout ROM that is independent of the Velocity movment
Rigidity
Mukhang sinapian
Opisthotonus
UMNL is the first order neurons regulated by the
neurotransmitter___
glutamate
what is spaticity
Slow passive movement will not elicit the increased
resistance
A velocity dependent increase in mm resistance to
a passive stretch
brisk stretches of mm will cause an abrupt inc in tone followed by a dec in mm resistance c continued stretch
Clasp knife rigidity
Affects the antigravity mm of arms and legs (flexors
of the arm and extensors of leg)
UMNL
in umnl Patients often exhibit flexor and extensor ____
spasms
- Ex. Stroke pts: UE is in flexion while LE is
in extension
What is clonus?
A sequence of rhythmic, involuntary mm cxn that occur at a frequency of ___
5-7 Hz
Occurs as a response to abruptly applied stretch
stimuli
clonus
where does clonus Most easily elicited at?
the ankle c brisk dorsiflexion and
plantar flexion movements
Patient can be seen to have abnormally brisk
reflexes which are d/t decreased modulation by
descending inhibitory pathways
Hyperreflexia of the DTR
: the tensing of abs
by stroking the overlying skin
Superficial abdominal reflex
the elevation of scrotum in
response to stroking medial thigh
Cremasteric reflex
what is synkinesia
Involuntary movements in limb that have
associations c the voluntary movements in other
limbs
flexion of arm may result in flexion of leg is an example of
synkinesia
____ can occur when yawning or sneezing
synkinesia
Volitional movements of one arm or leg may result
in mirror movements of opposite limb
synkinesia
Most CN have bilateral innervation from the brain,
with the exception of CN 7 & 12
Pseudo-Bulbar Palsy
Sx of pseudo-bulbar palsy
Slurred speech, dysphagia, dysarthria, brisk jaw
jerk, spastic tongue, and speudobulbar affect
Damaged alpha motor neuron → produces
spontaneous action potentials
Fasciculation, lmnl
These spikes cause the muscle fibers that are part
of the neuron’s motor unit to fire, resulting in visible
twitch of the affected mm.
fasciculation
Because ____ are the only way to
stimulate extrafusal muscle fibers, the loss of these
neurons causes a decrease in mm tone
alpha motor neurons
Hyporeflexia
- Myotatic (stretch reflex) is weak or absent c LMN
d/o because the ____that cause
mm contraction are damaged
alpha motor neurons
Where is the lesion for UMNL?
Above the anterior
horn in the SC or
above the nuclei of
the CN
Where is the lesion for LMNL?
Anterior horn cell,
motor nn fiber or
neuromuscular
junction
Where is the mm weakness in UMNL?
LE: All muscle groups (more
marked in the flexors)
UE: distally > proximally (Both flex & ext) (bec. UE ay usually naka-flex, so yung extensors di nag-cocontract, pero counterproductive rin kasi lagi namang nag-cocontract yung flexors)
Where is the mm weakness in LMNL?
distally>proximally. (Both
flexors and extensors affected)
Fasciculation in UMNL
absent
Fasciculation in LMNL
May be present in anterior horn cell
2 Major categories of stroke:
Ischemic
Hemorrhagic
Caused by a vascular occlusion
Ischemic
Caused by bleeding within the Parenchyma
of the brain
Hemorrhagic
Artery
pt deficit: CL weakness and sensory loss primarily in the LE, incontinence, aphasia, memory and behavioral deficits
Anterior cerebral Artery
Artery
pt deficit: CL sensory loss and
weakness in face and UE
Less involvement in LE,
homonymous hemianopia
Middle cerebral Artery
Artery
pt deficit: Ataxia, equilibrium,
disturbances, headaches,
dizziness
Vertebrobasilar Artery
> balance
Artery pt deficit: CL sensory loss, thalamic pain syndrome, homonymous hemianopsia, visual agnosia, and cortical blindness
Posterior cerebral Artery
> for Vision
> Related sila ng vertebrobasilar
(without vision, nawawala visuospatial awareness)
TRAUMATIC BRAIN INJURY (TBI) Are classified as ___, wherein the skull is ____.
Closed Head Injuries, not actually penetrated
nature of the injury sustained in vehicular accidents and falls (e.g., blunt impact, acceleration-deceleration) often results in multifocal lesions and diffuse brain damage with a variety of physical, cognitive, and neurobehavioral impairments that are unique to each person and pose formidable obstacles to community integration
TBI
● Clinical assessment of coma was made more precise
and objective _____
Glasgow Coma Scale (GCS)
GCS for Eye opening
Spontaneous
Opens eyes on own
4
GCS for Best motor response
Pain
Pulls examiner’s hands away when pinched
5
GCS for Eye opening
Speech
Opens eyes when asked in a loud voice
3
GCS for Eye opening
Pain
Opens eyes when pinched
2
GCS for Eye opening
Pain
Does not open eyes
1
GCS for Best motor response
Pain
Pulls a part of the body away when pinched
4
GCS for Best motor response
Pain
Flexes body inappropriately when pinched (decorticate posturing)
3
GCS for Best motor response
Pain
Body becomes rigid in an extended position when pinched (decerebrate posturing)
2
GCS for Best motor response
Pain
Has no motor response to pinch
1
GCS for Verbal response (talking)
Speech Carries on conversation correctly and tells examiner where he or she is, month and year
5
GCS for Verbal response (talking)
Speech Seems confused or disoriented
4
GCS for Verbal response (talking)
Speech Talks so examiner can understand victim but makes no sense
3
GCS for Verbal response (talking)
Speech Makes sounds that examiner cannot understand
2
GCS for Verbal response (talking)
Speech Makes no noise
1
Best and lowest score for GCS
BEST score to achieve: 15
○ Lowest is 3
VERBAL
○ What is your name? Where are you? What
month is it?
■ If they answer all >
“ORIENTATED”
○ What is your name? Where are you? What
month is it?
■ If pt speaks in incomplete sentences
> “CONFUSED”
○ What is your name? Where are you? What
month is it?
■ If talking gibberish/ swearing at
you >
“WORDS”
○ What is your name? Where are you? What
month is it?
■ moaning/groaning and can’t
make out what they are saying >
“SOUNDS”
○ What is your name? Where are you? What
month is it?
■ If there’s no response
> “NONE”
○ What is your name? Where are you? What
month is it?
■ If there is a tube on pt’s mouth >
“NOT TESTABLE (NT)”
○ Grasping and releasing fingers or opening
the mouth and sticking out the tongue >
“OBEYS COMMANDS”
○ Trapezius pinch (central stimulus), and
assess what their response is
■ If trapezius gives no response >
go to Supraorbital notch and test
that area
○ Trapezius pinch (central stimulus), and
assess what their response is
■ If they move their arm/hand up
above clavicle towards stimulus >
“LOCALISING” to pain
○ Trapezius pinch (central stimulus), and
assess what their response is
■ If arm bends and moves rapidly
away from body and stimulus >
“NORMAL FLEXION”
○ Trapezius pinch (central stimulus), and
assess what their response is
■ Elbow bends slowly and arm
comes across body >
“ABNORMAL FLEXION
“(Decorticate )
*Counterpart of Decorticate is
“ABNORMAL EXTENSION”
Decerebrate
○ Trapezius pinch (central stimulus), and
assess what their response is
■ No response
> “NONE”
○ Trapezius pinch (central stimulus), and
assess what their response is
■ If paralyzed
> “indicate NT” (not
testable)
Pathophysiology of TBI
● Primary TBI
■ Ex. nauntog sa dashboard, yung rebound
effect non
○ Damage that occurs directly and immediately as a
result of trauma to the brain. Cortical contusion
and DAI are the 2 subtypes of primary injury.
○ Cerebral contusion is the other main type of
primary injury. These cortical bruises commonly
occur at the crests of the gyri and extend to
variable depths, depending on severity.
○ Contusions often occur on the undersurface of
the frontal lobes, as well as the frontal and
temporal tips, regardless of the site of impact, due
to the internal architecture of the skull.
○ Coup-contrecoup injuries are more likely seen
when the moving head hits a stationary object,
such as with a fall. In this situation, one may see a
contusion at the site of impact as well as another,
often larger, contusion on the opposite cortex
distinguishing feature of TBI. Acceleration-deceleration and rotational forces that commonly result from motor vehicle accidents produce diffuse axonal disruption.
Diffuse Axonal Injury (DAI)
primarily responsible for the initial loss of consciousness
Diffuse Axonal Injury (DAI)
○ Any damage to brain tissue that takes place after the initial (primary) injury
Secondary TBI
■ Nanggaling sa primary TBI/ remnant ng
primary TB
____ are examples of intracellular processes that lead to secondary injury, but can be driven by factors taking place at the tissue or systemic level.
Apoptosis and excitotoxicity
○ Systemic factors such as anemia, hypotension,
pulmonary injury, and cardiac or respiratory arrest
also may contribute to secondary injury by
diminishing the delivery of oxygen to the injured
brain
Cerebral Hypoperfusion is assessed by
evaluating the _____
Cerebral Perfusion Pressure (CPP),
-the difference between mean arterial pressure (MAP) and intracranial pressure (ICP)
○ Factors that increase ICP or decrease MAP can
decrease CPP, leading to increased ischemic
injury.
■ ICP: di nag fflow maayos yung dugo, and
nag p-pile up lang siya sa isang area
Cerebral Perfusion Pressure
(CPP), which is defined as the
difference between
mean arterial pressure (MAP) and intracranial
pressure (ICP)
Glasgow Outcome Scale-Extended
1
Dead
Glasgow Outcome Scale-Extended
Dead
1
Glasgow Outcome Scale-Extended
2
Vegetative state (VS)
No cerebral cortical function that can be judged by
behavior (not able to follow simple commands or
communicate)
Glasgow Outcome Scale-Extended
3
Lower severe disability (lower SD)
Glasgow Outcome Scale-Extended
4
Upper severe disability (upper SD)
Need supervision/assistance in ADL, but can be alone for >8h/d
Glasgow Outcome Scale-Extended
5
Lower moderate disability (lower MD)
Independent in adl and can shop and travel indep on
public transportation, but has not returned to previous
position or lifestyle
Glasgow Outcome Scale-Extended
6
Upper moderate disability (upper MD)
Able to resume previous position or lifestyle with
alternative/modified duties or part-time d/t injury
Glasgow Outcome Scale-Extended
7
Lower good recovery (lower GR)
Able to resume previous position or lifestyle (may be
modified), but reporting some problems
Glasgow Outcome Scale-Extended
8
Upper good recovery (upper GR)
Complete return to previous lifestyle with no reported
problems
Glasgow Outcome Scale-Extended
Vegetative state (VS)
No cerebral cortical function that can be judged by
behavior (not able to follow simple commands or
communicate)
2
Lower severe disability (lower SD)
3
Upper severe disability (upper SD)
Need supervision/assistance in ADL, but can be alone for >8h/d
4
Lower moderate disability (lower MD)
Independent in adl and can shop and travel indep on
public transportation, but has not returned to previous
position or lifestyle
5
Upper moderate disability (upper MD)
Able to resume previous position or lifestyle with
alternative/modified duties or part-time d/t injury
6
Lower good recovery (lower GR)
Able to resume previous position or lifestyle (may be
modified), but reporting some problems
7
Upper good recovery (upper GR)
Complete return to previous lifestyle with no reported
problems
8
A complex, multifactorial dse that requires the expertise
of neurologists, physiatrists, OTs, and PTs, as well as
other participants in patient care
MULTIPLE SCLEROSIS
MS is a Autoimmune disease that is occurs twice as often in ___than ___
● Also appears to involve genetic factors c HLA-DR2 in
DR-positive families- having a greater chance of
developing the dse
women > men
Hallmark of MS Pathology:
Presence of:
- multifocal plaques (lesions) of demyelination in the cerebral hemispheres,
- optic nn
- brain stem, and
- spinal cord
Cardinal Symptoms (Charcot’s Triad):
SIN
○ Scanning speech
○ Intention tremor
○ Nystagmus
○ Characterized by discrete attacks of neurological
deficits (relapse) with either full or partial recovery
(remission) in subsequent weeks to months
■ To be considered a relapse, symptoms
must occur for more than 24 hours
■ Attacks for <24 hrs: pseudo- ng MS
○ The periods between relapses are characterized
by lack of disease progression
○ The stable patient may have local inflammatory
activity that is clinically silent
○ Affects approximately 85% of patients with MS at
diagnosis
● Relapsing-Remitting MS (RRMS)
○ Characterized by an initial relapsing-remitting
course, followed by a change in clinical course
with progression to steady and irreversible
decline with or without continued acute
attacks
○ May be the result of progressive axonal loss
rather than new lesions
○ Before newer treatments, the majority of patients
with RRMS progressed to SPMS
● Secondary-Progressive MS (SPMS)
○ Characterized by disease progression and steady
functional decline from onset; patients may
experience modest fluctuations in neurological
disability but discrete attacks do not occur
○ PPMS is associated with later onset (mean age
40 years) and more equal gender distribution
○ Affects approximately 10% of patients with MS
● Primary-Progressive MS (PPMS)
○ Characterized by a steady deterioration in
disease from onset (similar to PPMS) but with
occasional acute attacks.
○ Intervals between attacks are characterized by
continuing disease progression
○ Affects approximately 5% of patients with MS
○ Poor prognosis
● Progressing-Relapsing MS (PRMS)
