Motor system
May 23, 2017
Types of neurotransmitters
 There are many different ways to classify neurotransmitters. Dividing them into
amino acids, peptides, and monoamines is sufficient for many purposes.
 Some more precise divisions are as follows:
 Around 10 "small-molecule neurotransmitters" are known:
 acetylcholine (Ach)
 monoamines (epinephrine (E), norepinephrine (NE), dopamine (DA), serotonin (5-HT)
and melatonin)
 3 or 4 amino acids, depending on exact definition used: (primarily glutamic acid,
gamma aminobutyric acid (GABA), aspartic acid & glycine)
 Purines, (Adenosine, ATP, GTP and their derivatives)
 Fatty acids are also receiving attention as the potential endogenous cannabinoid.
 Over 50 neuroactive peptides (vasopressin, somatostatin, neurotensin, etc.)
have been found, among them hormones such as Luteinizing hormone (LH) or
insulin that have specific local actions in addition to their long-range signalling
properties.
 Histamine
 Single ions, such as synaptically released zinc, are also considered
neurotransmitters by some.
 Gaseous, including nitric oxide (NO) and carbon monoxide (CO)
 The major "workhorse" neurotransmitters of the brain are glutamic acid and
GABA.
What’s the motor system?
 Parts of CNS and PNS specialized for
control of limb, trunk, and eye movements
 Also holds us together
 From simple reflexes (knee jerk) to voluntary
movements (96mph fast ball)
Introduction
 Skeletal muscle contraction is
initiated by lower motor
neuron
 Lower motor neuron is a part
of local reflex circuits
 The information from several
sources is integrated in the
lower motor neuron
 Higher levels of CNS
 Upper motor neuron,
tectum, n. ruber, brain
stem
 Proprioception
http://www.frontiersin.org/files/Articles/42416/fnhum
HTML/image_m/fnhum-07-00085-g001.jpg
Lower motor neuron α motoneuron
 Innervation of
contractile elements
 Extrafusal fibers
 Muscle contraction
 γ motoneuron
 Innervation of muscle
spindles
 Intrafusal fibers
 Alignment of muscle
spindles
 Gamma loop
 β motoneuron
http://epomedicine.com/wp-content/uploads/2016/07/gamm
Alpha motor neurons (α-MNs)
 are large lower motor neurons of the brainstem and
spinal cord. They innervate extrafusal muscle fibers of
skeletal muscle and are directly responsible for initiating
their contraction.
 Alpha motor neurons are distinct from gamma motor
neurons, which innervate intrafusal muscle fibers of
muscle spindles.
 While their cell bodies are found in the central nervous
system (CNS), alpha motor neurons are also considered
part of the somatic nervous system—a branch of the
peripheral nervous system (PNS)—because their axons
extend into the periphery to innervate skeletal muscles.
Motor unit
 A typical muscle is
innervated by about 100
motoneurons which are
localized in motor
nucleus
 Each motoneuron
innervate from 100 to
1000 muscle fibers and
one muscle fiber is
innervated by a single
motoneuron
 The ensemble of muscle
fibers innervated by a
single neuron and
corresponding
motoneuron constitutes
the motor unit
Motor unit
 An alpha motor neuron
and the muscle fibers it
innervates is a motor
unit. A motor neuron
pool contains the cell
bodies of all the alpha
motor neurons involved
in contracting a single
muscle.
Patellar reflex
Stretch reflex
http://www.slideshare.net/ananthatiger/cns-4
Flexion withdrawal
reflex
12
 Polysynaptic reflex mediated by FRAs
(flexion reflex afferents: nociceptors,
mechanoreceptors etc.)
 flexion in response to painful stimuli
 FRAs synapse on inhibitory and
excitatory interneurons which excite
ipsilateral flexor motorneurons &
inhibit extensor motorneurons
 Physiological importance:
 Rapid flexion away from painful
stimuli
 Clinical importance: upper motor
neuron lesion impairs flexion reflex 
pathalogical Babinski sign
Upper motor neuron lesion:
Babinski sign
13
(Type of flexion
reflex)
(pathological reflex)
Whelan PJ. Shining light into
the black box of spinal
locomotor networks.
Philosophical Transactions of
the Royal Society of London
B: Biological Sciences.
2010;365:2383–2395.
Hierarchic organization of
motor system
http://www.slideshare.net/drpsdeb/pres
entations
Steps in Motor Action
Cortex
 Externally
guided
movements –
those requiring
sensory inputs
 Picking up
objects, using
tools, moving
eyes to explore
faces, making
gestures etc.
Voluntary motor activity
Idea
Associatio
n cortex
Premotor +
Motor cortex
Basal
Ganglia
Lateral
cerebellu
m
Movemen
t
Intermedia
te
Cerebellum
ExecutionPlanning
http://www.slideshare.net/drpsdeb/pres
entations
Voluntary motor activity
 Result of cooperation of
upper and lower motor
neuron
 Basal ganglia
 Motor gating – initiation of
wanted and inhibition of
unwanted movements
 Cerebellum
 Movement coordination
http://www.slideshare.net/drpsdeb/pres
 Upper motor neuron
 Primary motor cortex
 Lower motor neuron
 Anterior horn of spinal cord
 Tractus corticospinalis
lateralis
 90% of fibers
 Tractus corticospinalis
anterior
 10% of fibers
 Cervical and upper thoracic
segments
 Tractus corticobulbaris
Pyramidal
tract
http://images.slideplayer.com/14/4330915/slides/slide_34.jpg
Primary motor cortex
http://www.emunix.emich.edu
Motor cortex Primary motor cortex (area 4)
 Somatotopic organization
 Control of lower motor neuron
 Premotor cortex (area 6
laterally)
 Preparation of strategy of
movement
 Sensor motor transformation
 Movement patterns selection
 Supplementary motor cortex
(area 6 medially)
 Involved in planning of complex
movements
 Movement of both limbs
 Complex motion sequences
 Activated also by complex
movement rehearsal
http://www.slideshare.net/CsillaEgri/prese
The primary motor cortex
 (or M1) works in association with pre-motor areas to plan and
execute movements.
 M1 contains large neurons known as Betz cells which send long
axons down the spinal cord to synapse onto alpha motor
neurons which connect to the muscles.
 Pre-motor areas are involved in planning actions (in concert
with the basal ganglia) and refining movements based upon
sensory input (this requires the cerebellum).
 The human primary motor cortex is located in the dorsal part
of the precentral gyrus and the anterior bank of the central
sulcus. The precentral gyrus is in front of the postcentral gyrus
from which it is separated by the central sulcus. Its anterior
border is the precentral sulcus, while inferiorly it borders to the
lateral fissure (Sylvian fissure). Medially, it is contiguous with the
paracentral lobule.
Motoric controlling systems
 The upper motor neurons
reside in the precentral
gyrus of the frontal lobe also
called the "motor strip".
These upper motor neurons
are arranged in a
stereotypical fashion.
Neurons which control
movements of the face and
mouth are located near the
Sylvian or lateral fissue and
neurons which control the
muscles of the thighs and
legs are located near the
medial longitudinal fissure
and within the central
sulcus.
Major Motor Pathways
1. Corticospinal (cortex
to spinal cord)
a) Lateral – distal limb
muscles (fine
manipulations)
b) Ventral – trunk and
upper leg muscles
(posture/locomotion)
2. Corticobulbar (cortex
to pons, 5th, 7th, 10th
and 12th cranial nerves)
– control of face and
tongue muscles; upper
face both contralateral,
lower face contralateral
Major Motor Pathways
3. Ventromedial
(brain stem to
spinal cord) – trunk
and proximal limb
muscles (posture,
sneezing, breathing,
muscle tone)
4. Rubrospinal (red
nucleus to spinal
cord) – modulation
of motor movement
(limb movement
independent of
trunk movement)
Pyramidal Motor System
Corticobulbar tract
 Upper motor neurons which innervate the muscles of
the face and head are located near the lateral fissure
of the brain.
 Their axons coalesce to form the corticobulbar tract.
 These axons then descend within the genu of the
internal capsule to the medial part of the cerebral
peduncle.
 The upper motor neuron axons then synapse on lower
motor neurons of the cranial nerve nuclei which are
located in midbrain, pons and medulla.
Corticospinal Tract
Motor neuron lesions
29
 Upper motor neuron lesion of the neural
pathway inside the CNS (not including the
ventral horn of the spinal cord or motor nuclei
of the cranial nerves)
 stroke, traumatic brain injury or cerebral
palsy
 Lower motor neuron lesion affects nerve
fibers within the ventral horn of the spinal cord
travelling to the relevant muscle(s)
 Nerve trauma, polio
Upper motor
neuron lesion
Lower motor
neuron lesion
Reflexes Increased, may have
pathological reflex
signs (Babinski sign)
Decreased,
Muscle
tone
Increased,
contralateral
Decreased,
ipsilateral
Weakness Yes, contralateral Yes, ipsilateral
Paraplegia
 is an impairment in motor and/or sensory function of the
lower extremities. It is usually the result of spinal cord
injury or a congenital condition such as spina bifida
which affects the neural elements of the spinal canal.
 The area of the spinal canal which is affected in
paraplegia is either the thoracic, lumbar, or sacral
regions. If the arms are also affected by paralysis,
tetraplegia is the proper terminology.
 The causes range from trauma (acute spinal cord injury:
transsection or compression of the cord, usually by bone
fragments from vertebral fractures) to tumors (chronic
compression of the cord), myelitis transversa and
multiple sclerosis.
Hemiplegia
 It can be congenital (occurring before, during, or soon
after birth) or acquired (as from illness or stroke).
 It is usually the result of a stroke, although disease
processes affecting the spinal cord and other diseases
affecting the hemispheres are equally capable of
producing this clinical state. Hemiplegia can be a more
serious consequence of stroke than spasticity.
 Other causes include Type 2 diabetes mellitus, which
can lead to transient hemiplegia, a type of spinal injury
called Brown-Sequard syndrome, and injections of local
anaesthetic given intra-arterially rapidly, instead of given
in a nerve branch.
 Lesions in the posterior limb of the internal capsule can
also lead to hemiplegia.
Damage to Parietal
Lobe
 Superior region important in visual
guided movements
 Damage to superior regions can
produce optic ataxia
 Optic ataxia – difficulty in using
visual information to guide actions
that cannot be ascribed to motor,
somatosensory, or visual-field or –
acuity deficits.
 Afferent paresis – loss of
kinesthetic feedback that results
from lesions to the postcentral
gyrus and produces clumsy
movements
Apraxia
 Apraxia – an inability to perform skilled, sequential,
purposeful movement
 This cannot be accounted by disruptions in more basic
motor processes such as muscle weakness, abnormal
posture or tone, or movement disorder (e.g., chorea).
 Two pieces of evidence that apraxia is a higher order
disorder:
1. It occurs bilaterally (lower level deficits are contralateral to
the side of the injury)
2. Individuals can perform behaviours spontaneously but not
when imitating someone or on verbal command
Oral (buccofascial)
Apraxia vs. Limb Apraxia
 Oral apraxia is
associated with
difficulties performing
voluntary movements
with the muscles of
the tongue, lips,
cheek, larynx
 Limb apraxia disrupts
the ability to use
limbs to manipulate
items such as
screwdrivers, scissors
or hammers.
Ideational vs. Ideomotor
Apraxia
 Ideational apraxia – difficulty in performing
a movement when the “idea” of the
movement is lost
 It occurs when individuals can perform simple
one-step movement but not multistep
movement
 Ideomotor apraxia – difficulty in performing
a movement when a disconnection occurs
between the idea of movement and its
execution
 Simple movements of an abstract nature are
most affected
Other Apraxias
 Constructional apraxia –
individuals cannot manipulate
objects correctly with regards
to their spatial relations (e.g.,
wooden block arrangement)
 Dressing apraxia –
individuals have difficulty
manipulating and orienting
clothing and limbs so that the
clothing can be put on
correctly
 Callosal apraxia – difficulty
with manipulating and using
the left hand after verbal
instructions (language in the
left hemisphere)
Extrapyramidal Motor System
 The extrapyramidal system dampens erratic motions, maintains
muscle tone and truncal stability. It is phylogenetically older that
the pyramidal system and thus plays a relatively more important
role in lower animals. Many of its synaptic connections are
extremely complex and even today, poorly understood.
Neurodegenerative disorders which affect the extrapyramidal
system have yielded much of our knowledge about its normal
function.
 The major parts of the extrapyramidal system are the "subcortical
nuclei". This includes the caudate, putamen, and globus pallidus
which are also known as the Basal ganglia. The caudate nucleus
is especially affected in Huntington's chorea.
 The substantia nigra, is located in the midbrain. It is particularly
affected in idiopathic Parkinson's disease.
Extrapyramidal system: synapses and neurotransmission
Extrapyramidal Motor System
 The thalamus is a very complex structure with many functions
including cognition and pain perception, but parts of the
thalamus are also components of the extrapyramidal system.
 Other nuclei include the Subthalamic nucleus. Unilateral damage
to the subthalamic nucleus results in hemiballism.
 The final major nucleus is the Red Nucleus which is immediately
adjacent to the substantia nigra in the midbrain.
 To summarize, the extrapymidal nuclei include the substantia
nigra, caudate, putamen, globus pallidus, thalamus, red nucleus
and subthalamic nucleus. All of these nuclei are synaptically
connected to one another, the brainstem, cerebellum and the
pyramidal system.
Basal Ganglia
 Unlike the cerebellum,
which plays a role in rapid
balistic movements, the
basal ganglia are more
important for the
accomplishment of
movements that may take
some time to initiate or
stop
 Important for internal
guiding (rather then
external) of movement
 Dopamine – nigrostriatal
pathway
Basal Ganglia
Damage to the basal ganglia:
 Produces either too much
activation (hyperkinetic)
responses= twitches,
movements bursts, jarring, etc.
 Huntington’s Chorea-dominant
gene based, increases
glutamate in striatum which
destroys GABA neurons in BG
and loss of inhibition
 No cure
 Tourette’s
OR
 Produces too little force
(hypokinetic)=rigidity
 Parkinson’s disease Pink=inhibition
Blue=excitation
Disorders of the basal ganglia
46
Parkinson’s Disease
 Parkinson's Disease is the second most
common age-related neurodegenerative
disease, affecting
approximately 1% of population over 60.
 Characterized by resting tremor,
slowed/absent movement
(hypokinesia), rigidity of the
extremities and neck, & reduced facial
expressiveness
 Caused by the loss of the dopaminergic
neurons in the substantia nigra pars
compacta
 Typically treated with L-Dopa
Parkinson's Disease (PD)
 Emerging evidence has provided support for the
hypothesis that PD is the result of complex
interactions between genetic abnormalities,
environmental toxins, mitochondrial dysfunction and
other cellular processes.
 Recently, epigenetic modifiers have been identified
as a potential mediators of environmental factors
participating in the pathogenesis of PD
Parkinson's Disease
 Although the exact cause of Parkinson's disease is
unknown, research has concentrated on genetics,
environmental toxins, endogenous toxins and viral
infection.
In Parkinson's, cells are destroyed in part of the brain
stem - the substantia nigra, which sends out fibers to the
corpus stratia, gray and white bands of tissue in both
sides of the brain. Cells there release dopamine, one of
three major neurotransmitters (chemical messengers)
which help the body respond to stress. By the time
symptoms develop, patients have lost 80 to 90 percent
of their dopamine-producing cells.
Parkinson’s Disease
50
Increased output of indirect
pathway, decreased output of direct
pathway
Parkinson's Disease
 Symptoms include tremors, slowed
movement and postural instability.
 Other features include rigidity, flexed posture,
freezing phenomenon and loss of postural
reflexes.
 Patients can experience depression, sleep
disturbances, dizziness and problems with
speech, swallowing and sexual functioning.
PD pathogenesis
 PD is characterized by accumulation of SNCA in the
presynaptic nerve terminals of dopaminergic neurons in the
SN. The neurotoxicity of SNCA might be mediated through
interaction with histone altering its acetylation.
 Hyperacetylation of H3 or H4 represents key epigenetic
changes in dopaminergic neurons. Some environmental
toxins have been found to induce a time-dependent
increase or decrease of histone acetylation of DNA
(Dieldrin, paraquat).
 Dysregulation of acetylation of H3 or H4 is regarded as an
important mechanism underlying pesticide-induced neuron
loss in PD.
Journal of the Neurological Sciences 349 (2015) 3-9
Possible role of DNA methylation and
related factors in the pathogenesis
of PD.
One-carbon metabolic disturbance
results in decreased level of Sadenosylmethionine
(SAM), which
leads to hypomethylation of DNA.
The decreased methylation level of
specific PD-related genes changes
chromosome conformation and
makes much easier for transcription,
such as SNCA overexpression that
leads to α-synuclein accumulation
and subsequently dopaminergic
neurons degeneration. In addition,
high level of homocysteine (HCY)
can induce dopaminergic neuronal
apoptosis via impairment of
mitochondrial function and
apoptosis-related gene activation,
leading to caspase activation and
neuronal apoptosis. AIF, apoptosis
inducible factor; Met, methionine;
SAH, S-adenosylhomocysteine.
Journal of the Neurological Sciences 349 (2015) 3-9
The process of histone
acetylation and its effect on
gene transcription.
Two main enzymes termed
as acetylase (HATs) and
deacetylase (HDACs)
mediate the process of
acetylation/deacetylation,
respectively. The histone
acetylation produced a
more loosened chromatin
structure leading to
transcriptional activation,
whereas histone
deacetylation formed
heterochromatin and then
transcriptional repression.
TF, transcriptional factor;
RN-p, RNA polymerase.
Journal of the Neurological Sciences 349 (2015) 3-9
Huntington's disease
 Huntington's disease is caused by a trinucleotide repeat expansion
in the Huntingtin gene, which codes for Huntingtin protein,
denoted "Htt". Huntington's disease is one of several polyglutamine
diseases. This expansion produces an altered form of the Htt
protein, called mutant Huntingtin (mHtt), the misfunction of this
protein increases neuronal cell death in select areas of the brain.
This damage itself isn't fatal, but life expectancy is reduced due to
complications caused by its symptoms.
 Huntington's disease's most obvious symptoms are abnormal body
movements called chorea and a lack of coordination, but it also
affects a number of mental abilities and some aspects of
behavior. Physical symptoms occur in a large range of ages
around a mean occurrence of late forthies/early fifties, but if they
occur before the age of 20 then the condition is known as Juvenile
HD. As there is currently no proven cure, symptoms are managed
with various medications and supportive services.
Huntington's disease
 Huntington's disease is caused by a trinucleotide repeat expansion
in the Huntingtin gene, which codes for Huntingtin protein,
denoted "Htt". Huntington's disease is one of several polyglutamine
diseases. This expansion produces an altered form of the Htt
protein, called mutant Huntingtin (mHtt), the misfunction of this
protein increases neuronal cell death in select areas of the brain.
This damage itself isn't fatal, but life expectancy is reduced due to
complications caused by its symptoms.
 Huntington's disease's most obvious symptoms are abnormal body
movements called chorea and a lack of coordination, but it also
affects a number of mental abilities and some aspects of
behavior. Physical symptoms occur in a large range of ages
around a mean occurrence of late forties/early fifties, but if they
occur before the age of 20 then the condition is known as Juvenile
HD. As there is currently no proven cure, symptoms are managed
with various medications and supportive services.
Huntington´s disease-genetics
 Normal state
 DNA
 ATGCAGGTGACCTCAGTG
 TACGTCCACTGGAGTCAC
 RNA
 AUGCAGGUGACCUCAGUG
 PROTEIN
 Met-Gln-Val-Thr-Ser-Val
 Trinucletide expansion mutation
 DNA
 ATG(CAGCAGCAG)20CAGGTGACCTC
AGTG
 TAC(GTCGTCGTC)20GTCCACTGGAGT
CAC
 RNA
 AUG
(CAGCAGCAG)20CAGGUGACCUCAG
UG
 PROTEIN
 Met-(Gln-Gln-Gln)20Gln-Val-Thr-Ser-Val
Pathophysiology of HD
 Degeneration of neuronal cells, especially in the frontal lobes
and caudate nucleus (the striatum) of the basal ganglia occurs.
There is also astrogliosis and loss of medium spiny neurons.
 In Huntington's disease the external globus pallidus over-inhibits
the flow of excitation from the subthalamic nuclei, which
interferes with the initiation of motion. The subthalamic nuclei
also generate reduced excitation to the internal globus pallidus,
resulting in a weak inhibitory signal to the thalamus. The thalamus
in turn then sends a strong excitatory signal to the putamen
resulting in unmodulated motion.
 Role of epigenetics still unclear (but probable)
Cerebellum
 The cerebellum, which located inferior to the
tentorium, coordinates muscle activity,
equilibrium and tone.
 It is functionally and anatomically divided into
three lobes. The flocculonodular lobe or
archicerebellum maintains equilibrium.
 The anterior lobe or paleocerebellum maintains
muscle tone.
 The posterior lateral lobes or neocerebellum
controls coordination and allows us to perform
intricate motor tasks like playing the piano.
Recent evidence suggests that the
neocerebellum also plays a role in memory,
especially memory of fine motor skills.
 Cebebellar motor tracts are uncrossed, so that
injuries on one side will cause difficulties on the
same side of the body.
 The major cerebellar tracts are the
 Spinocerebellar, connecting the spinal cord and the
cerebellum,
 Vestibulospinal, connecting the vestibular system and
the cerebellum,
 Corticopontocerebellar, connecting the cortex, pons
and cerebellum and the
 Dentatorubrothalamic connecting the dentate nucleus
of the cerebellum, the red nucleus and the thalamus.
Cerebellum:
inputs
63
Receive many inputs
from periphery, spinal
cord and brain
regions
Cerebellum:
outputs
64
Vestibular system
 The vestibular system controls balance. It is synaptically linked to
the extrapyramidal system. So that persons with extrapyramidal
neurodenerative disorders frequently also have problems with
balance and may experience frequent falls.
 The semicircular canals are lined by hair cells and filled with
endolymph. The endolymph moves when the head moves and
thus stimulates the hair cells. The hair cells then project
synaptically to the Vestibular ganglion which is located within the
bone of the skull. The ganglion then sends projections to the
Superior and lateral vestibular nuclei which are located in the
medulla adjacent to the base of the fourth ventricle. These nuclei
in turn send axons via the Inferior cerebellar peduncle to the
Flocculonodular lobe of the cerebellum to maintain equilibrium.
Vestibular system
 The major tracts of the vestibular system include
the lateral vestibulospinal which maintains
equilibrium, the vestibuloocular which controls
saccadic eye movements and the
vestibulocortical which causes dizziness when
stimulated.
 The practical implications are that diseases of the
inner ear cause loss of equilibrium, dizziness and
saccadic eye movements when the head is
turned.
Tremor
Tremor
 is an unintentional, somewhat rhythmic,
muscle movement involving to-and-fro
movements (oscillations) of one or more parts
of the body.
 It is the most common of all involuntary
movements and can affect the hands, arms,
head, face, vocal cords, trunk, and legs. Most
tremors occur in the hands. In some people,
tremor is a symptom of another neurological
disorder.
Tremor
 is generally caused by problems in parts of the
brain or spinal cord that control muscles
throughout the body or in particular areas, such
as the hands.
 Neurological disorders or conditions that can
produce tremor include multiple sclerosis, stroke,
traumatic brain injury and neurodegenerative
diseases that damage or destroy parts of the
brainstem or the cerebellum.
 Other causes include the use of some drugs (such
as amphetamines, caffeine, corticosteroids, and
drugs used for certain psychiatric disorders,
alcohol abuse or withdrawal, mercury poisoning,
overactive thyroid or liver failure.
Tremor
 is generally caused by problems in parts of the
brain or spinal cord that control muscles
throughout the body or in particular areas, such
as the hands.
 Neurological disorders or conditions that can
produce tremor include multiple sclerosis, stroke,
traumatic brain injury and neurodegenerative
diseases that damage or destroy parts of the
brainstem or the cerebellum.
 Other causes include the use of some drugs (such
as amphetamines, caffeine, corticosteroids, and
drugs used for certain psychiatric disorders),
alcohol abuse or withdrawal, mercury poisoning,
overactive thyroid or liver failure.
Tremor
 Tremors can be an indication of hypoglycemia, along with
palpitations, sweating and anxiety. A magnesium and
Vitamin B1 deficency has also been known to cause a
tremor or shaking, soon resolved when the nutrients are
taken.
 Tremor may occur at any age but is most common in
middle-aged and older persons. It may be occasional,
temporary, or occur intermittently. Tremor affects men and
women equally.
Tremor classification
 Tremor is most commonly classified by clinical features and cause or
origin. Some of the better known forms of tremor, with their
symptoms, include the following:
 Essential tremor (sometimes called benign essential tremor) is the
most common of the more than 20 types of tremor. The hands are
most often affected but the head, voice, tongue, legs, and trunk
may also be involved. Head tremor may be seen as a “yes-yes” or
“no-no” motion.
Essential tremor may be accompanied by mild gait disturbance.
Tremor frequency may decrease as the person ages, but the
severity may increase, affecting the person’s ability to perform
certain tasks or activities of daily living.
Heightened emotion, stress, fever, physical exhaustion, or low blood
sugar may trigger tremors and/or increase their severity. Onset is
most common after age 40, although symptoms can appear at any
age. It may occur in more than one family member. Children of a
parent who has essential tremor have a 50 percent chance of
inheriting the condition. Essential tremor is not associated with any
known pathology.
Tremor classification
 Parkinsonian tremor is caused by damage to
structures within the brain that control movement.
This resting tremor, which can occur as an isolated
symptom or be seen in other disorders, is often a
precursor to Parkinson's disease (more than 25
percent of patients with Parkinson’s disease have
an associated action tremor).
The tremor, which is classically seen as a “pill-rolling”
action of the hands that may also affect the chin,
lips, legs, and trunk, can be markedly increased by
stress or emotions. Onset of parkinsonian tremor is
generally after age 60. Movement starts in one limb
or on one side of the body and usually progresses
to include the other side.
Tremor classification
 Dystonic tremor occurs in individuals of all ages who
are affected by dystonia, a movement disorder in
which sustained involuntary muscle contractions
cause twisting and repetitive motions and/or painful
and abnormal postures or positions.
Dystonic tremor may affect any muscle in the body
and is seen most often when the patient is in a
certain position or moves a certain way. The
pattern of dystonic tremor may differ from essential
tremor. Dystonic tremors occur irregularly and often
can be relieved by complete rest. Touching the
affected body part or muscle may reduce tremor
severity (a geste antagoniste). The tremor may be
the initial sign of dystonia localized to a particular
part of the body.
Tremor classification
 Psychogenic tremor (also called hysterical tremor)
can occur at rest or during postural or kinetic
movement. The characteristics of this kind of
tremor may vary but generally include sudden
onset and remission, increased incidence with
stress, change in tremor direction and/or body
part affected, and greatly decreased or
disappearing tremor activity when the patient is
distracted. Many patients with psychogenic
tremor have a conversion disorder or another
psychiatric disease.
Tremor classification
 Orthostatic tremor is characterized by fast (>12Hz)
rhythmic muscle contractions that occur in the
legs and trunk immediately after standing.
Cramps are felt in the thighs and legs and the
patient may shake uncontrollably when asked to
stand in one spot. No other clinical signs or
symptoms are present and the shaking ceases
when the patient sits or is lifted off the ground. The
high frequency of the tremor often makes the
tremor look like rippling of leg muscles while
standing. Orthostatic tremor may also occur in
patients who have essential tremor.
Tremor classification
 Physiologic tremor occurs in every normal individual and
has no clinical significance. It is rarely visible to the eye and
may be heightened by strong emotion (such as anxiety or
fear), physical exhaustion, hypoglycemia, hyperthyroidism,
heavy metal poisoning, stimulants, alcohol withdrawal or
fever.
 It can be seen in all voluntary muscle groups and can be
detected by extending the arms and placing a piece of
paper on top of the hands. Enhanced physiologic tremor is
a strengthening of physiologic tremor to more visible levels.
It is generally not caused by a neurological disease but by
reaction to certain drugs, alcohol withdrawal, or medical
conditions including an overactive thyroid and
hypoglycemia. It is usually reversible once the cause is
corrected.
The degree of tremor should be assessed in four positions. The tremor can
then be classified by which position most accentuates the tremor:
Position Name Description
At rest Resting tremors Tremors that are worse at rest include
Parkinsonian syndromes and essential tremor if
severe. This includes drug-induced tremors
from blockers of dopamine receptors such as
haloperidol and other antipsychotic drugs.
During contraction (eg. a tight fist
while the arm is resting and
supported)
Contraction
tremors
Tremors that are worse during supported
contraction include essential tremor and also
cerebellar and exaggerated physiologic
tremors such as a hyperadrenergic state or
hyperthyroidism
[1]
. Drugs such as adrenergics,
anti-cholinergics, and xanthines can
exaggerate physiologic tremor.
During posture (eg with the arms
elevated against gravity such as in a
'bird-wing' position)
Posture tremors Tremors that are worse with posture against
gravity include essential tremor and
exaggerated physiologic tremors
[1]
.
During intention (eg finger to nose
test)
Intention tremors Intention tremors are tremors that are worse
during intention, e.g. as the patient's finger
approaches a target, including cerebellar
disorders
Thank you for your attention