Exam 2 Flashcards
Movement disorders are neuro disorders related to ___ dysfunction. Resulting movement disorders are either hyper or hypo___. Hypo___ Movement Disorders include __ and __. Hyper__ movement disorders include __, __, __, and __.
Movement disorders are neuro disorders related to BASAL GANGLIA dysfunction. Resulting movement disorders are either hyper or KINETIC. HYPOKINETIC Movement Disorders include PARKINSON’S DISEASE and PARKINSON’S PLUS SYNDROMES. HYPERKINETIC movement disorders include CHOREA, ATHETOSIS, BALLISM, and DYSTONIA.
Pyramidal signs are thought to be related to the __ system and were thought to control [voluntary/ involuntary] mvmt. Extrapyramidal signs are thought to be related to the ___ and were thought to be related to [voluntary/ involuntary] mvmt.
Pyramidal signs = CORTICOSPINAL System, VOLUNTARY movement
Extrapyramidal signs = BASAL GANGLIA, INVOLUNTARY movement
The primary role of the BG is to ___ [internally generated / externally provoked] movements. It changes ___ as the task demands change.
The primary role of the BG is to INITIATE INTERNALLY-GENERATED movements. It changes MOTOR SETS as the task demands change.
The Basal Ganglia refers to [cortical/ sub cortical] [gray/white] matter including the __, __, and __. Functionally, it also includes the __.
The Basal Ganglia refers to SUBCORTICAL GRAY matter including the CAUDATE, PUTAMEN, & GLOBUS PALLIDUS. Functionally, it also includes the SUBSTANTIA NIGRA.
The striatum is composed of the nucleus ___, ___, and ___.
The striatum is composed of the NUCLEUS ACCUMBENS, CAUDATE NUCLEUS, & PUTAMEN
The lentiform nucleus consists of the ___ and ___.
The lentiform nucleus consists of the PUTAMEN & GLOBUS PALLIDUS
The globus pallidus has 2 sections: __ and __.
Globus Pallidus has 2 sections: External Segment (GPe) and Internal Segment (GPi).
The Substantia Nigra is located in the [midbrain/ pons/ medulla] and consists of the ___ (___ part) and ___ (___ part).
The Substantia Nigra is located in the MIDBRAIN and consists of the PARS COMPACTA (SNc) (DOPAMINE part) and PARS RETICULATA (SNr) (RETICULA part).
The Subthalamic nucleus is associated with the [mesencephalon/ diencephalon/ telencephalon]
The Subthalamic nucleus is associated with the DIENCEPHALON
The striatum (aka __) is composed of the __ and __, which are from [the same/ different] embryological origin(s). As the ___ develops, it grows around in the wall of the [3rd/4th/ lateral] ventricles into a __-shape. The __ forms the [inner/outer] most part (medial/lateral) of the ___ nucleus. The projection neurons in this area use ___ as their neurotransmitter, so they’re [excitatory/inhibitory] on their targets. The striatum is the [output/receiving] area of the basal ganglia, [getting/sending] input from all areas of the __ and ___. The [dorsal/ventral] part of the striatum is the ___ which is related to the __ system.
The striatum (aka NEOSTRIATUM) is composed of the CAUDATE and PUTAMEN, which are from THE SAME embryological origin(s). As the CAUDATE develops, it grows around in the wall of the LATERAL ventricles into a C-shape. The PUTAMEN forms the OUTER most part LATERAL of the LENTIFORM NUCLEUS. The projection neurons in this area use GABA as their neurotransmitter, so they’re INHIBITORY on their targets. The striatum is the RECEIVING area of the basal ganglia, GETTING input from all areas of the CORTEX and THALAMUS. The VENTRAL part of the striatum is the NUCLEUS ACCUMBENS which is related to the LIMBIC system.
The globus pallidus forms the [medial/lateral] part of the ___ nucleus. It is divided into __ and __ segments and uses __ as its neurotransmitter, so it has a [phasic/tonic] [excitatory/ inhibitory] effect on the __. It is one of the two [inflow/ outflow] nuclei of the BG.
The globus pallidus forms the MEDIAL part of the LENTIFORM nucleus. It is divided into INTERNAL and EXTERNAL segments and uses GABA as its neurotransmitter, so it has a TONIC INHIBITORY effect on the THALAMUS. It is one of the two OUTFLOW nuclei of the BG.
The pars reticulata (SNr) is the [dorsal/ventral] part of the substantia nigra, adjacent to the ___. It uses __ as its neurotransmitter, so it has a [phasic/tonic] [excitatory/inhib] effect on its targets which are the __ and areas of the brainstem. It is one of the two [inflow/ outflow] nuclei of the BG.
The pars reticulata (SNr) is the VENTRAL part of the substantia nigra, adjacent to the CRUS CEREBRI. It uses GABA as its neurotransmitter, so it has a TONIC INHIBITORY effect on its targets which are the THALAMUS and areas of the brainstem. It is one of the two OUTFLOW nuclei of the BG.
The sublthalamic nucleus (STN) lies [dorsal/ventral] to the thalamus, and [medial/lateral] to the internal capsule. It uses ___ as a neurotransmitter, so it is [excitatory/inhibitory]. It is involved in the [indirect/ direct] circuits of the BG.
The sublthalamic nucleus (STN) lies VENTRAL to the thalamus, and MEDIAL to the internal capsule. It uses GLUTAMATE as a neurotransmitter, so it is EXCITATORY. It is involved in the INDIRECT circuits of the BG.
The substantia nigra pars compacta (SNc) is the [dorsal/ventral] part of the substantia nigra. The neurons in this region contain the pigment __. This region uses __ as its neurotransmitter (and it also makes it!) and projects to the ___ to set the background level of __.
The substantia nigra pars compacta (SNc) is the DORSAL part of the substantia nigra. The neurons in this region contain the pigment NEUROMELANIN. This region uses DOPAMINE as its neurotransmitter (and it also makes it!) and projects to the STRIATUM to set the background level of EXCITABILITY.
The basal ganglia has two pathways through which it activates desired movement and inhibits all other motor programs.
Direct: ___ > ___> ___ (__, __)
(Direct action: _____)
Indirect: ___ > ___ > ___> ___ > ___ (__, __)
(Indirect action: _____)
The basal ganglia has two pathways through which it activates desired movement and inhibits all other motor programs.
Direct: Striatum > Gpi> Thalamus (VL, Vim)
(Direct action: ACTIVATES DESIRED MOTOR PROGRAM)
Indirect: Striatum > Gpe > STN> Gpi > Thalamus (VL, Vim)
(Indirect action: INHIBITS COMPETING PROGRAMS)
At rest, the thalamus is [quiet/firing]. The direct circuit contributes to this via the ___ neuron that projects to the thalamus [phasically/tonically] __-__x/second with the neurotransmitter ___ to [excite/inhibit] it. The indirect circuit acts via the ___ to [phasically/tonically] [inhibit/excite] the ___.
At rest, the thalamus is QUIET. The direct circuit contributes to this via the GPi neuron that projects to the thalamus TONICALLY 1-2x/second with the neurotransmitter GABA to INHIBIT it. The indirect circuit acts via the GPe to TONICALLY INHIBIT the STN.
Direct circuit during movement:
The ___ [inhibits/excites] the striatum. The striatum then actively [excites/inhibits] the [excitation/ inhibition] (aka ___) from the GPi, which [allows the thalamus to fire/ makes the thalamus quiet] and recruit a motor program in the cortex.
Direct circuit during movement:
The CORTEX EXCITES the striatum. The striatum then actively INHIBITS the INHIBITION (aka DISINHIBITION) from the GPi, which ALLOWS THE THALAMUS TO FIRE and recruit a motor program in the cortex.
Indirect circuit during movement:
The cortex excites the ___, which then has an [excitatory/ inhibitory] effect on the GPe, which in turn [excites/inhib] the [excitatory/ inhibitory] effect of the GPe on the ___, rendering it [active/quiet]. The __ then [excites/inhibits] GPi neurons which then [excite/inhibit] the thalamus to inhibit competing motor programs in the cortex.
The cortex excites the STRIATUM (caudate) which then has an INHIBITORY effect on the GPe, which in turn INHIBITS the INHIBITORY effect of the GPe on the STN, rendering it ACTIVE. The STN then EXCITES GPi neurons which then INHIBIT the thalamus to inhibit competing motor programs in the cortex.
The [direct/indirect] circuit of the basal ganglia activates the desired motor program in the cortex, and the [direct/indirect] circuit inhibits undesired motor programs.
The DIRECT circuit of the basal ganglia activates the desired motor program in the cortex, and the INDIRECT circuit inhibits undesired motor programs.
Dopamine is generated by the ___. There are ___ (#) different types of dopamine receptors, so its role is complex.
Dopamine is generated by the SUBSTANTIA NIGRA PARS IMPACTA. There are 5 (#) different types of dopamine receptors, so its role is complex.
[GABA/Glutamate/Dopamine] sets the background level of excitation in the striatum. Too much of this neurotransmitter results in ___, and too little of it results in ___.
DOPAMINE sets the background level of excitation in the striatum. Too much of this neurotransmitter results in DYSKINESIAS, and too little of it results in AKINESIA.
Dopamine bursts interact with input from the __ to ___ neurons during learning and promotes long term ___. This means that as you ___, the inputs are more easily activated. Dopamine may act to focus attention to a particular ensemble of __ neurons.
Dopamine bursts interact with input from the CORTEX to STRIATAL neurons during learning and promotes long term POTENTIATION. This means that as you LEARN MORE, the CORTICAL inputs are more easily activated. Dopamine may act to focus attention to a particular ensemble of STRIATAL neurons.
The ___ is the outflow nucleus of the BG that has significant brainstem connections and it also projects to the thalamus. Specifically, it projects to the ___ and to the __ and ___ to affect walking and muscle tone.
The SUBSTANTIA NIGRA PARS RETICULATE (SNr) is the outflow nucleus of the BG that has significant brainstem connections and it also projects to the thalamus. Specifically, it projects to the SUPERIOR COLLICULUS and to the MESENCEPHALIC LOCOMOTOR REGION (MLR) and Pedunculopontine nucleus (PPN) to affect walking and muscle tone.
Basal ganglia projections through the SNr to the ___ drive CPGs in the spinal cord for walking. This connection affects rhythmic stepping & the initiation & termination of locomotion. The BG projections through the SNr to the ___ influences muscle tone areas of the BS reticular formation. Without normal BG input through these systems, postural muscle tone [incr/decr].
Basal ganglia projections through the SNr to the MLR drive CPGs in the spinal cord for walking. This connection affects rhythmic stepping & the initiation & termination of locomotion. The BG projections through the SNr to the PPN influences muscle tone areas of the BS reticular formation. Without normal BG input through these systems, postural muscle tone INCREASES.
The BG affects walking via the ___. This drives ___ in the spinal cord for locomotion and affects ___ stepping, and the __ and __ of locomotion.
The BG affects walking via the MESENCEPHALIC LOCOMOTOR REGION (MLR). This drives CENTRAL PATTERN GENERATORS in the spinal cord for locomotion and affects RHYTHMIC stepping, and the INITIATION & TERMINATION of locomotion.
The BG affects muscle tone via the ___ in areas that control muscle tone. Without normal BG influence, muscle tone [incr/decr] leading to [rigidity/spasticity/flaciddity].
The BG affects muscle tone via the RETICULAR FORMATION in areas that control muscle tone. Without normal BG influence, muscle tone INCREASES leading to RIGIDITY
The BG affects eye movements via the ___. It allows it to generate [smooth pursuit/ saccades/ nystagmus/ gaze fixation].
The BG affects eye movements via the SUPERIOR COLLICULUS. It allows it to generate SACCADIC EYE MOVEMENTS
The cortico-BG loop (upstream) is more responsible for [volitional/ automatic] movements. The BG-Brainstem loop (downstream) is more responsible for [volitional/ automatic] movements such as __ and __.
The cortico-BG loop (upstream) is more responsible for VOLITIONAL (deliberate) movements. The BG-Brainstem loop (downstream) is more responsible for AUTOMATIC movements such as GAIT, MUSCLE TONE, EYE MOVEMENTS.
The BG has a number of roles in Motor Control. It generates [externally-cued/ internally-triggered] movements. It is especially active with [well-established motor programs/ newly learned & novel movements]. Specifically, the [Cb/ BG} helps to establish motor programs initially, then it shifts to the {Cb/BG]. The BG plays a role in flexibly selecting and shifting between ___ as the task demand changes (think of the spotlight on each task!). It serves as an important gate for the processing of ___ information and how to use that in motor control. Specifically, it selects relevant ___ and suppresses irrelevant information before executing an action. Finally, the BG has a role in cognitive-related functions, allowing you to focus your attention on a ___ & maintain safe mobility during multiple ongoing motor & cognitive tasks.
The BG has a number of roles in Motor Control. It generates INTERNALLY-TRIGGERED movements. It is especially active with WELL-ESTABLISHED MOTOR PROGRAMS (OVERLEARNED MVMTS) Specifically, the CEREBELLUM helps to establish motor programs initially, then it shifts to the BG. The BG plays a role in flexibly selecting and shifting between MOTOR SETS as the task demand changes (think of the spotlight on each task!). It serves as an important gate for the processing of SENSORY information and how to use that in motor control. Specifically, it selects relevant SENSORY INFO and suppresses irrelevant information before executing an action. Finally, the BG has a role in cognitive-related functions, allowing you to focus your attention on a PRIMARY TASK & maintain safe mobility during multiple ongoing motor & cognitive tasks.
Non-motor functions of the BG involve switching ___ between tasks. The ___ (part of the BG) regulates ___ behavior (e.g. ___). The [dorsal/ventral] striatum is involved with ___-based behaviors related to ___. It projects to the ___ cortex and is affected by [GABA/ Glutamate/ Dopamine].
Non-motor functions of the BG involve switching ATTENTION between tasks. The CAUDATE (part of the BG) regulates COMPULSIVE behavior (e.g. OCD). The VENTRAL striatum is involved with REWARD-based behaviors related to ADDICTION. It projects to the FRONTAL cortex and is affected by DOPAMINE.
Lesions in the BG appear clinically [ipsilateral/ contralateral] to the side of the lesion because the ___ tract [does/does not] cross.
Lesions in the BG appear clinically CONTRALATERAL to the side of the lesion because the CORTICOSPINAL tract CROSSES.
Parkinson’s disease (aka ___) occurs due to a loss of ___ cells of the ___. Symptoms do not appear until __-__% of these cells are lost. Degeneration occurs for a number of reasons, but the most likely etiology of PD is a combination of accelerated __, ___ predisposition, exposure to ___, and an abnormality in __ mechanisms. Specifically, there is likely oxygen free radical damage that results in an accumulation of __ in dopaminergic neurons in the __.
Parkinson’s disease (aka PARALYSIS AGITANS) occurs due to a loss of DOPAMINERGIC cells of the SUBSTANTIA NIGRA PARS COMPACTA (SNc). Symptoms do not appear until 70-80% of these cells are lost. Degeneration occurs for a number of reasons, but the most likely etiology of PD is a combination of accelerated AGING, GENETIC predisposition, exposure to TOXINS, and an abnormality in OXIDATIVE mechanisms. Specifically, there is likely oxygen free radical damage that results in an accumulation of LEWY BODIES in dopaminergic neurons in the SNc.
In PD, we see onset between __-__yo, slightly more in [men/women], and __x more in whites than blacks. The prevalance in North America is __ or __% of the >65yo population. ___ (#) new cases are seen per year.
In PD, we see onset between 40-70yo, slightly more in MEN, and 4X more in whites than blacks. The prevalance in North America is 1 MILLION or 1% of the >65yo population. 60,000 (#) new cases are seen per year.
Clinical features of PD include… (4)
(1) RESTING pill rolling tremor (4-6Hz)
(2) Bradykinesia & poverty of movement (loss of facial expression, difficulty initiating movement, increased latency to onset of voluntary mvmt, loss of reciprocal mvmt [eg arm swing in gait], decreased amplitude & speed of mvmts, micrographia [tiny handwriting])
(3) COG-WHEEL rigidity (not velocity dependent, incr resistance on both sides of jt. Series of catches & releases)
(4) Loss of Equilibrium & postural reflexes (NOT one of the 3 clinical diagnostic features!)
To receive a dx of PD, a patient must have 2 of the following:
- ___
- ____
- ___
…AND a consistent response to ____ replacement therapy.
To receive a dx of PD, a patient must have 2 of the following:
- RESTING TREMOR
- BRADYKINESIA & POVERTY OF MVMT
- COG-WHEEL RIGIDITY
…AND a consistent response to L-DOPA replacement therapy.
We see a number of motor control impairments with PD. Patients may have difficulty generating [externally/internally] triggered movements, making them more dependent on [internal/external] cues. They will have [fast/slowed] movements, aka ___, accompanied by [incr/decr] amplitude of body & eye movements, [incr/decr] BOS, and [incr/decr] arm swing. We also might see ___, which is related to a difficulty switching between motor programs. This movement hesitation results in a delay or complete inability to initiate a step and is a major contributor to __. This occurs most often when navigating a ___ environment. We also see ___ gait which is difficulty [initiating/terminating] gait. These patients have difficulty with sensory organization, meaning they are unable to filter __ from __ from th eenvironment and can’t use ___ in useful ways. This misselection results in an [over/under]estimation of amplitude of movement, resulting in ___. Posturally, we’ll see a [flexed/extended] position with [incr/decr/normal] trunk rotation. Their impaired postural control is affected by reduced __ especially backwards, rigidity of the __, bradykinesia, and lack of appropriate or effective __ in response to perturbation. We see impaired __ movements, including [hypo/hyper] metric saccades and a breakdown of __. Finally we see cognitive & limbic impairments, including difficulty in ___ attention and __-task situations as well as concurrent __ and /or dementia as the disease progresses.
We see a number of motor control impairments with PD. Patients may have difficulty generating INTERNALLY- triggered movements, making them more dependent on EXTERNAL cues. They will have SLOWED movements, aka BRADYKINESIA, accompanied by DECREASED amplitude of body & eye movements, NARROWED BOS, and DECREASED arm swing. We also might see FREEZING, which is related to a difficulty switching between motor programs. This movement hesitation results in a delay or complete inability to initiate a step and is a major contributor to FALLS. This occurs most often when navigating a COMPLEX environment. We also see FESTINATING gait which is difficulty TERMINATING gait. These patients have difficulty with sensory organization, meaning they are unable to filter RELEVENT from IRRELEVENT SENSORY CUES from the environment and can’t use PROPRIOCEPTION in useful ways. This misselection results in an OVERestimation of amplitude of movement, resulting in RIGIDITY. Posturally, we’ll see a FLEXED position with DECREASED trunk rotation. Their impaired postural control is affected by reduced LIMITS OF STABILITY especially backwards, rigidity of the TRUNK, bradykinesia, and lack of appropriate or effective POSTURAL RESPONSES in response to perturbation. We see impaired EYE movements, including HYPO metric saccades and a breakdown of SMOOTH PURSUIT. Finally we see cognitive & limbic impairments, including difficulty in DIVIDED attention and DUAL-task situations as well as concurrent DEPRESSION and /or DEMENTIA as the disease progresses.
Secondary impairments from PD may include __ or __ and may contribute to mobility difficulties. Late-stage PD may be accompanied by __ dysfunction, including __, __, and __; as well as __ disturbances.
Secondary impairments from PD may include CONTRACTURES or LOSS OF THORACIC MOBILITY & DECR RESPIRATORY EXCURSION and may contribute to mobility difficulties. Late-stage PD may be accompanied by AUTONOMIC dysfunction, including ORTHOSTASIS, DECR BOWEL MOTILITY, and URINARY FREQUENCY; as well as SLEEP disturbances.
Rating scales for PD include the ___ and the __.
Rating scales for PD include the HOEHN & YAHR and the UNITED PARKINSON DISEASE RATING SCALE (UPDRS).
Medical management of PD generally starts with ___, but this becomes ineffective after a while. Later, they will try ___ replacement therapy. Drug treatment is generally delayed as long as possible because of the side effects that develop after ___-__ years on the meds. ___ can develop when the meds peak because the receptors are so sensitive to it, and you may see dramatic __ times. ___ can have dramatic effects on PD functioning; this is commonly done in ___ (area of brain).
Medical management of PD generally starts with DOPAMINE AGONIST (MIRAPEX), but this becomes ineffective after a while. Later, they will try L-DOPA replacement therapy. Drug treatment is generally delayed as long as possible because of the side effects that develop after 3-5 years on the meds. DYSKINESIAS can develop when the meds peak because the receptors are so sensitive to it, and you may see dramatic ON-OFF times. DEEP BRAIN STIMULATION can have dramatic effects on PD functioning; this is commonly done in SUBTHALAMIC NUCLEUS (area of brain).
Parkinson’s Plus Syndromes is differentially-diagnosed between PD and other degenerative disorders that may present with one or more PD-related signs like tremor or bradykinesia. However, 2 differentiating features of Parkinson’s Plus Syndromes:
(1) They are not responsive to ____
(2) They progress [faster/slower] than PD
They include…(5)
Parkinson’s Plus Syndromes is differentially-diagnosed between PD and other degenerative disorders that may present with one or more PD-related signs like tremor or bradykinesia. However, 2 differentiating features of Parkinson’s Plus Syndromes:
(1) They are not responsive to DOPAMINE
(2) They progress FASTER than PD
They include... Multiple System Atrophy (MSA) Progressive Supranuclear Palsy (PSP) Corticobasal Degeneration Lewy Body Dementia Olivopontocerebellar Atrophy
Chorea is a type of ___ and occurs because of damage to the __. Symptoms include a serious of continuous [fast/slow] movements of the __, __, and ___ especially the __ and __. These movements usually resemble fragments of functional movements and they’re [voluntary/ involuntary].
Chorea is a type of DYSKINESIA and occurs because of damage to the STRIATUM. Symptoms include a serious of continuous FAST movements of the FACE, TONGUE & DISTAL LIMBS, especially FINGERS & TOES. These movements usually resemble fragments of functional movements and they’re INVOLUNTARY.
Athetosis is a type of ___ and occurs because of damage to the __. Symptoms include [fast/slow] ___ movements, that are ___-like. It involves more of the [distal/whole] limbs compared to chorea.
Athetosis is a type of DYSKINESIA and occurs because of damage to the STRIATUM. Symptoms include SLOW WRITHING movements, that are SNAKE-like. It involves more of the WHOLE limbs compared to chorea.
__ is an intermediate form between chorea and athetosis
CHOREOATHETOSIS
Hemiballismus is a type of ___ that results from damage to the __. It may be the result of a ___ involving a small branch of the [anterior/posterior] [cerebral/cerebellar] artery. Symptoms include ___ movements usually of [one/both] arm or leg.
Hemiballismus is a type of DYSKINESIA that results from damage to the SUBTHALAMIC NUCLEUS. It may be the result of a STROKE involving a small branch of the POSTERIOR CEREBRAL artery. Symptoms include VIOLENT FLAILING movements usually of ONE arm or ONE leg.
Huntington’s Chorea is a ___ genetic disorder, meaning you have a __% chance of inheritance. It’s allele is located on chromosome __ and consists of an extended (>___(#)) ___ trinucleotide repeat. Genetic testing is available. We see a profound loss of interneurons (spiny neurons) in the __ and __, as well as reactive __ in the striatum. There is also neuronal loss in the __ and ___, so these patients have [cognitive/motor/both] impairments. The ventricles are [shrunken/enlarged/normal]. Cell death in Huntington’s is thought to be due to an accumulation of oxygen free radicals or failure of __ energy metabolism.
Huntington’s Chorea is a AUTOSOMAL DOMINANT genetic disorder, meaning you have a 50% chance of inheritance. It’s allele is located on chromosome 4 and consists of an extended (>40 REPEATS) CAG trinucleotide repeat. Genetic testing is available. We see a profound loss of interneurons (spiny neurons) in the CAUDATE & PUTAMEN, as well as reactive GLIOSIS in the striatum. There is also neuronal loss in the CORTEX and CEREBELLUM, so these patients have BOTH COGNITIVE AND MOTOR impairments. The ventricles are ENLARGED. Cell death in Huntington’s is thought to be due to an accumulation of oxygen free radicals or failure of MITOCHONDRIAL energy metabolism.
Huntington’s Disease is a [common/rare] disease, affecting __(#)/100,000. The mean age of onset is __-__.
Huntington’s Disease is a RARE disease, affecting 6.5/100,000. The mean age of onset is 35-42
Huntington’s disease often presents with [motor/cognitive] changes, including ___, ___, ___, and subtle changes in ___ as well as choreoathetotic movements in the __. Chorea advances [proximally/distally]. We see ataxic gait with chorea and choreoathetotic movements of the __ and __. Cognitive changes including __ and __ are also seen.
Huntington’s disease often presents with COGNITIVE changes, including _DEPRESSION, IRRITABILITY, SLOWED COGNITION, DECR ABILITY TO PROBLEM SOLVE and subtle changes in COORDINATION as well as choreoathetotic movements in the FINGERS. Chorea advances PROXIMALLY We see ataxic gait with chorea and choreoathetotic movements of the FACE and TONGUE. Cognitive changes including DEPRESSION & DEMENTIA are also seen.
Diagnostic testing for Huntington’s includes…
- Genetic testing
- MRI/CT: reduced volume in striatum
- PET scan: Reduced D1 & D2 binding
SPECT: reduced blood flow in the caudate>putamen
Cerebral palsy defines a group of disorders with common factors including abnormal ___, early onset (generally __ or ___), and absence of recognized underlying ___ disease. Common associated features may include __, ___ impairment, __ and __-motor abnormalities, __, and __ and __ impairments.
Cerebral palsy defines a group of disorders with common factors including abnormal MOTOR CONTROL, early onset (generally PRENATAL or PERINATAL), and absence of recognized underlying PROGRESSIVE disease (SO THE ETIOLOGY IS UNKNOWN!). Common associated features may include SEIZURES, COGNITIVE impairment, VISUAL and VISUO-motor abnormalities, DEAFNESS, and SPEECH & LEARNING impairments.
Name the Subclassifications of CP…(4)
(1) Spastic
(2) Extrapyramidal (related to BG damage)
(3) Hypotonic (floppy, low tone; not typical)
(4) Mixed & atypical types
Spastic CP is secondary to a [LMN/UMN] problem and is accompanied by [hyper/hypo]reflexia. We see abnormal __ reflexes and dominant __ reflexes. These patients have sustained __ and tone in their __. Spastic CP is further classified by topography (part of the brain affected and includes:
(1) Hemiplegia: impacting [part/whole] of one hemisphere
(2) Spastic diplegia: damage to [medial/lateral] part of ___ affecting [one/both] [UE/LE]
(3) Spastic quadriplegia: [smaller/bigger] hemorrhage affecting all 4 limbs
(4) : Monoplegia: hemmorhage on [one/both] sides, usually affecting [UE/LE]
(5) Triplegia: due to a [symmetrical/asymmetrical] bleed
Spastic CP is secondary to a UMN problem and is accompanied by HYPERreflexia. We see abnormal POSTURAL reflexes and dominant TONIC NECK reflexes. These patients have sustained CLONUS and tone in their ADDUCTORS. Spastic CP is further classified by topography (part of the brain affected and includes:
(1) Hemiplegia: impacting ALL of one hemisphere
(2) Spastic diplegia: damage to MEDIAL PORTION OF INTERNAL CAPSULE affecting BOTH LE
(3) Spastic quadriplegia: BIGGER hemorrhage affecting all 4 limbs
(4) : Monoplegia: hemmorhage on ONE side, usually affecting LE
(5) Triplegia: due to a ASYMMETRICAL bleed
Extrapyramidal CP is related to damage to the ___. We see __, __, and ___ subtypes.
Extrapyramidal CP is related to damage to the BG. We see ATHETOSIS, CHOREA, AND CHORE-ATHETOTIC movements
