Disorders Of The Motor System

Front 1

Where does the voluntary motor system originate?

Back 1

The voluntary motor system originates in the motor areas of the frontal lobe cortex that send their output caudally in the corticospinal tract

Front 2

Anatomic Classification of Motor System Disease: Principal Disorders of the Motor System from Proximal to Distal: CENTRAL NERVOUS SYSTEM

Back 2

Corticospinal diseases (disorders of the upper motor neuron)
Extrapyramidal movement disorders
Cerebellar ataxias
Spinal cord diseases

Front 3

Anatomic Classification of Motor System Disease: Principal Disorders of the Motor System from Proximal to Distal: PERIPHERAL NERVOUS SYSTEM

Back 3

Radiculopathies and lower motor neuron diseases
Peripheral nerve disorders
Polyneuropathy
Focal neuropathy
Neuromuscular junction
Myasthenia
Lambert-Eaton myasthenic syndrome
Botulism
Muscular disorders

Front 4

The patient with motor system disease usually complains of __________

Back 4

difficulty with accomplishing specific tasks.

Front 5

Patients with central nervous system (CNS) disorders typically have difficulty with

Back 5

coordination, balance, and rapid movements

Front 6

CNS disorders: Muscle strength/tone

Back 6

Muscle strength is frequently normal, and muscle atrophy (wasting) is usually lacking. Muscle tone is usually increased, characterized by spasticity or rigidity.

Front 7

Patients with peripheral nervous system (PNS) disordersusually complain of difficulty with

Back 7

tasks

Front 8

PNS: proximal weakness= impairment in _____

Back 8

if weakness is proximal, there is impairment in climbing or descending stairs, rising from a chair, or lifting heavy objects above the head.

Front 9

PNS: distal weakness= impairment in ______

Back 9

If weakness is distal, then the patient complains of stumbling and tripping or of having problems fastening buttons or opening locks or doors with the hands.

Front 10

weakness vs fatigue

Back 10

A patient with weakness who is unfamiliar with what is taking place may use words such as numbness, deadness, tiredness, or fatigue. In contrast, when a patient complains of weakness, it often results from systemic rather than neurologic disease. In such patients, strength is often normal or only mildly reduced because the complaint is usually a loss of stamina and endurance. The patient with a complaint of fatigue should be asked to distinguish between true weakness and the less specific symptoms of lassitude and asthenia. If the patient is unable to perform a specific normal activity, then true weakness is suggested.

Front 11

If the patient is unable to perform a __________, then true weakness is suggested.

Back 11

specific normal activity

Front 12

Objective evidence of weakness is established if symptoms _________

Back 12

exceed the boundaries of normal variation (e.g., double vision, drooping eyelids, difficulty swallowing, repeated aspiration of food or liquids into the airway), as opposed to the more subjective complaints of inability to lift, carry, or push an object.

Front 13

CNS motor disorders can result from

Back 13

focal brain or spinal cord diseases such as those that occur with stroke, tumor, or inflammatory or demyelinating disease.

Front 14

Central motor systems are divided into three constituents

Back 14

pyramidal, extrapyramidal, and cerebellar

Front 15

CNS: pyramidal

Back 15

(named for the pyramidal cross-section of fiber tracts in the medulla)

is the major outflow from motor cortex to spinal cord.

Lesions of the pyramidal system cause motor weakness (paresis), spasticity, and hyperreflexia.

Although lesions of this system disturb motor function, they are not considered movement disorders.

Movement disorders are caused by extrapyramidal or cerebellar dysfunction

Front 16

Lesions of the pyramidal system cause

Back 16

motor weakness (paresis), spasticity, and hyperreflexia.

Front 17

Movement disorders are caused by

Back 17

extrapyramidal or cerebellar dysfunction

Front 18

CNS: extrapyramidal

Back 18

refers to the basal ganglia and their projections.

Front 19

The basal ganglia receive input from the

Back 19

cortex and give feedback to the cortex through projections from the thalamus

Front 20

The basal ganglia modulate

Back 20

motor cortical activity

activity of association cortex, particularly in the frontal lobes

Front 21

Many movement disorders involve complex ________

Back 21

Many movement disorders therefore involve complex

Front 22

Movement disorders entail either ___________________

Back 22

too little movement (hypokinesia) or too much movement (hyperkinesia)

Front 23

Rigidity

Back 23

increased muscular tone throughout the range of motion. It does not vary with passive acceleration of the limb by the examiner.

Front 24

Lead-pipe rigidity

Back 24

connotes the ductile quality of metal being passively bent

Front 25

Cogwheel rigidity

Back 25

the superimposition of tremor on underlying rigidity.

Front 26

Paratonic rigidity or paratonia

Back 26

velocity-dependent resistance to passive movement.

Such resistance increases as the speed of passive limb displacement increases.

Patients with paratonic rigidity demonstrate gegenhalten, an inability to fully relax a limb for passive range-of-motion testing.

This group of patients also demonstrates mitgehen, the tendency to help out as the examiner attempts to move the limb passively.

Paratonia is clinically nonspecific; it is common in patients with diminished cerebral function resulting from a variety of causes.

Front 27

True rigidity always implies

Back 27

basal ganglia dysfunction on the contralateral side.

Front 28

Descriptive Terms of the Hyperkinesias: Asterixis

Back 28

Transitory loss of motor tone resulting in rapid movement of a joint (the conceptual opposite of myoclonus)

Front 29

Descriptive Terms of the Hyperkinesias: Athetosis

Back 29

Slow writhing movement

Front 30

Descriptive Terms of the Hyperkinesias: Ballism

Back 30

Flailing movement (typically unilateral-hemiballism)

Front 31

Descriptive Terms of the Hyperkinesias: Chorea

Back 31

Irregular flicking, dancelike movement

Front 32

Descriptive Terms of the Hyperkinesias: Choreoathetosis

Back 32

The combination of chorea and athetosis

Front 33

Descriptive Terms of the Hyperkinesias: Dyskinesia

Back 33

Nonspecific term for hyperkinesia (generally chorea, athetosis, and dystonia, alone or in combination)

Front 34

Descriptive Terms of the Hyperkinesias: Dystonia

Back 34

Sustained contortion resulting from excess muscular activity across a joint: generalized, segmental, or focal

Front 35

Descriptive Terms of the Hyperkinesias: Myoclonus

Back 35

Rapid jerking muscular movement: multifocal or segmental, rhythmic or irregular

Front 36

Descriptive Terms of the Hyperkinesias: Tic

Back 36

Semi-suppressible motor or vocal gestural movement (may be simple, such as eye blinking or throat clearing, or complex, such as hopping or swearing)

Front 37

Descriptive Terms of the Hyperkinesias: Tremor

Back 37

Rhythmic oscillating movement: predominantly at rest or with action

Front 38

Signs of Cerebellar System Impairment:
Ataxia

Back 38

Poorly coordinated, broad-based, lurching gait

Front 39

Signs of Cerebellar System Impairment: Ataxic dysarthria

Back 39

Abnormal modulation of speech velocity and volume

Front 40

Signs of Cerebellar System Impairment: Dysmetria

Back 40

Irregular placement of voluntary limb or ocular movement

Front 41

Signs of Cerebellar System Impairment: Hypometria

Back 41

Movement falling short of the intended target

Front 42

Signs of Cerebellar System Impairment: Hypermetria

Back 42

Movement overshooting the intended target

Front 43

Signs of Cerebellar System Impairment: Dysdiadochokinesis

Back 43

Breakdown in precision and completeness of rapid alternating movements (as with a pronation-supination task)

Front 44

Signs of Cerebellar System Impairment: Dysrhythmokinesis

Back 44

Irregularity of the rhythm of rapid alternating movements or planned movement sequences

Front 45

Signs of Cerebellar System Impairment: Dyssynergia

Back 45

Inability to perform movement as a coordinated temporal sequence

Front 46

Signs of Cerebellar System Impairment: Hypotonia

Back 46

Decreased resistance to passive muscular extension (seen immediately after injury to the lateral cerebellum)

Front 47

Signs of Cerebellar System Impairment: Intention tremor

Back 47

Tremor orthogonal to the direction of intended movement (tends to increase in amplitude as the target is approached)

Front 48

Signs of Cerebellar System Impairment: Titubation

Back 48

Rhythmic rocking tremor of the trunk and head

Front 49

diagnostic criteria for Parkinson disease

Back 49

tremor
bradykinesia
muscular rigidity
postural instability

Front 50

underlying basis for Parkinson's disease

Back 50

Premature death of pigmented dopaminergic neurons in the pars compacta of the substantia nigra is the underlying basis of the disease, but the cause remains unclear.

Front 51

Clinical Features of Parkinson Disease: Primary Features

Back 51

Bradykinesia
rest tremor
rigidity
postural instability
therapeutic response to levodopa

Front 52

Clinical Features of Parkinson Disease: Secondary Features

Back 52

Masked facies (facial hypomimia)
Dysphagia; hypophonia or palilalia, micrographia, stooped posture, festinating gait, start hesitation, dystonic cramps
Autonomic dysfunction: orthostatic hypotension, urinary incontinence, constipation
Behavioral alterations: depression, dementia, sleep disorders including restless legs syndrome
Sensory complaints: aching, numbness, tingling

Front 53

Progression of Parkinson's symptoms

Back 53

The patient notes unilateral symptoms initially: characteristically, hand tremor, decreased arm swing, foot dragging, or micrographia.

Symptoms and signs subsequently spread to involve both sides.

Gradually worsening postural instability ultimately results in wheelchair confinement.

Symmetrical onset of symptoms and early falls caused by postural instability are atypical of idiopathic Parkinson disease, whereas they are common in other causes of the akinetic-rigid syndrome

Front 54

_________ remains the mainstay of treatment for advanced Parkinson disease.

Back 54

Carbidopa-levodopa (Sinemet) remains the mainstay of treatment for advanced Parkinson disease.

Front 55

Failure of bradykinesia and rigidity to improve in response to a trial of levodopa treatment raises the possibility _________

Back 55

of other disease processes because these diseases typically involve primary pathologic deterioration at the level of the striatum rather than the substantia nigra.

Front 56

Medications for Parkinson Disease: Anticholinergic Agents

Back 56

Trihexyphenidyl (Artane)
Benztropine (Cogentin)

Front 57

Medications for Parkinson Disease: Dopamine Precursors (Combined with Peripheral Aromatic Amino Acid Decarboxylase Inhibitors)

Back 57

Carbidopa-levodopa (Sinemet, Sinemet-CR, Parcopa) (regular, controlled-release, and orally disintegrating forms)
Benserazide-levodopa (Madopar) (marketed in Europe)

Front 58

Medications for Parkinson Disease: Dopamine Agonists

Back 58

Apomorphine (Apokyn) (injectable short acting), bromocriptine (Parlodel)
Pramipexole (Mirapex)
Rotigotine (Neupro) (transdermal patch)
Ropinirole (Requip, Requip XR)

Front 59

Medications for Parkinson Disease: Monoamine Oxidase Type B (MAO-B) Inhibitors

Back 59

Selegiline (deprenyl) (Carbex, Eldepryl, Zelapar)
Rasagiline (Azilect)

Front 60

Medications for Parkinson Disease: Catechol-O-Methyltransferase (COMT) Inhibitors

Back 60

Tolcapone (Tasmar)
Entacapone (Comtan)

Front 61

Medications for Parkinson Disease: Catechol-O-Methyltransferase (COMT) Inhibitors Combined with Carbidopa-Levodopa

Back 61

Entacapone-carbidopa-levodopa (Stalevo)

Front 62

Levodopa (dopamine precursor) requires __________ to dopamine within substantia nigra neurons

Back 62

requires enzymatic conversion to dopamine within substantia nigra neurons

Front 63

Unlike levodopa, the dopamine agonists do not compete with other _______ to cross the blood-brain barrier; they require no ____________ and act directly at the level of the striatum, bypassing the ___________.

Back 63

Unlike levodopa, the dopamine agonists do not compete with other amino acids to cross the blood-brain barrier; they require no enzymatic conversion and act directly at the level of the striatum, bypassing the substantia nigra.

Front 64

Concern with levadopa

Back 64

Concern has been expressed that treatment with levodopa may eventually provoke motor complications, such as on-off fluctuations and dyskinesias.

Front 65

Parkinsons therapy with be initiated with _______

Back 65

Initiating therapy with dopamine agonists allows the physician to reserve levodopa treatment for later stages of the illness.

Front 66

The co-administration of a ___________ in the later stages of illness may reduce the amount of levodopa required.

Back 66

dopamine agonist

Front 67

Selegiline

Back 67

Monoamine Oxidase Type B (MAO-B) Inhibitors

delays the need for levodopa treatment in patients with early Parkinson disease.

Selegiline inhibits monoamine oxidase type B, an enzyme that breaks down dopamine.

Toxic free radicals generated in the normal catabolism of dopamine may damage dopaminergic neurons in the substantia nigra, which may cause Parkinson disease in patients who are vulnerable as a result of a combination of inherited risk and as yet undetermined environmental exposures.

It has been postulated that selegiline may act as a neuroprotective agent if the formation of free radicals is inhibited

Front 68

Rasagiline

Back 68

second generation selective monoamine oxidase type B inhibitor.

Patients may tolerate it better because it is not metabolized to amphetamine (as compared to selegiline)

Front 69

The aromatic amino acid decarboxylase inhibitor carbidopa and the catechol-O-methyltransferase (COMT) inhibitors entacapone and tolcapone block the breakdown of ______

Back 69

Levadopa

Co-administration of levodopa with carbidopa and a COMT inhibitor suppresses levodopa's peripheral catabolism, maximizing the amount available to cross the blood-brain barrier and prolonging its effective half-life.

Tolcapone has been associated with rare but potentially lethal liver toxicity; the hepatic function of patients undergoing treatment with this drug must be monitored closely.

Entacapone has no adverse effect on liver function and is now in widespread use.

Front 70

Because enhancing _______________is the underlying rationale of drug treatments for Parkinson disease, most antiparkinsonian drugs have unwanted __________ side effects

Back 70

Because enhancing dopaminergic neurotransmission is the underlying rationale of drug treatments for Parkinson disease, most antiparkinsonian drugs have unwanted dopaminergic side effects.

Front 71

dopaminergic side effects of parkinsons treatment

Back 71

nausea, orthostatic hypotension, hallucinations, psychosis, and dyskinesia (i.e., abnormal involuntary hyperkinetic movements such as chorea and dystonia).

Front 72

The most common cause of drug-induced parkinsonism is treatment with _________________

Back 72

The most common cause of drug-induced parkinsonism is treatment with neuroleptic medication

Front 73

Drugs Causing Bradykinesia or Rigidity

Back 73

Established

Neuroleptics (virtually all phenothiazines, butyrophenones, others)
Metoclopramide
Tetrabenazine
Reserpine

Reported

Lithium
Phenytoin
Angiotensin-converting enzyme inhibitors

Front 74

Lewy body disease may be classified into three types based on the pathologic distribution of underlying Lewy bodies:

Back 74

brainstem, transitional, and diffuse

Front 75

Restriction of Lewy bodies to the brainstem defines _________________

Back 75

parkinson's disease

Front 76

Lewy body disease: Transitional phase

Back 76

Lewy bodies spread to involve the limbic system

Front 77

Lewy Body Disease: Diffuse phase

Back 77

clinical parkinsonism combined with prominent dementia occurs.

Visual hallucinations are common, patients may be extremely sensitive to the adverse effects of neuroleptic medication, and cognitive fluctuations occur

Front 78

PROGRESSIVE SUPRANUCLEAR PALSY

Back 78

gait disturbance, falls, bradykinesia, and rigidity.

Unlike patients with idiopathic Parkinson disease, patients with progressive supranuclear palsy typically do not have tremor.

A progressive loss of voluntary eye movements occurs with the preservation of oculocephalic reflex eye movements (the hallmark of a supranuclear eye movement abnormality).

Patients develop dementia, pseudobulbar affect (i.e., affective lability without correlative underlying emotional content), and frontal release signs.

Progression is faster than it is in patients with idiopathic Parkinson disease, and symptomatic response to dopaminergic agents is limited.

The cause of progressive supranuclear palsy remains unknown.

Tau-containing neurofibrillary tangles develop, with neuronal loss and gliosis involving the globus pallidus, subthalamic nucleus, substantia nigra, pons, oculomotor complex, medulla, and dentate nucleus of the cerebellum.

Front 79

CORTICOBASAL-GANGLIONIC DEGENERATION

Back 79

a tauopathy involving neurofibrillary tangles, neuronal loss, and gliosis.

Classically the disease manifests with marked asymmetry of motor dysfunction characterized by bradykinesia, rigidity, and apraxia (failure of learned motor movements) on one side of the body or in a single limb.

The "alien hand" syndrome can be a hallmark of the disorder; the limb adopts seemingly deliberate movements that are not under the direct voluntary control of the patient.

As the disease progresses, a combination of cortical dementia (aphasia, agnosia, apraxia) and basal-ganglia dysfunction (bradykinesia, rigidity, and postural instability, with or without tremor) becomes increasingly disabling.

Asymmetry persists late into the course.

Front 80

ESSENTIAL TREMOR

Back 80

This condition is inherited and ranges in severity from cosmetic to disabling.

Unlike the tremor of Parkinson disease, essential tremor typically affects both sides of the body symmetrically and is more prominent with action than it is at rest.

The frequency of the tremor oscillation is relatively constant, but the amplitude may vary.

As with all forms of tremor, stress, sleep deprivation, and stimulants (e.g., caffeine) make the condition worse.

Alcohol often relieves essential tremor

Essential tremor starts somewhat earlier than it does with Parkinson disease and may affect the neck and head muscles and the voice, as well as the arms and hands.

The most useful medications for essential tremor include propranolol (Inderal), primidone (Mysoline), and topiramate (Topamax).

DBS surgery with electrode placement in the ventral intermediolateral nucleus of the thalamus is highly effective but should be reserved for patients whose condition is refractory to pharmacotherapies.

Front 81

OTHER CAUSES OF TREMOR: Parkinson disease tremor

Back 81

is worse at rest, is often slower than essential tremor, and responds best to anticholinergic treatment rather than to medications for essential tremor

Front 82

OTHER CAUSES OF TREMOR: Cerebellar tremor

Back 82

has a more irregular rhythm, is coarser than either essential tremor or the tremor of Parkinson disease, and is more pronounced as the limb approaches a target (action tremor).

Front 83

OTHER CAUSES OF TREMOR: rubral tremor

Back 83

extremely coarse tremor with significant intention dysmetria that occurs with lesions in the area of the red nucleus in the mesencephalon.

Front 84

OTHER CAUSES OF TREMOR: drug induced tremor

Back 84

Numerous drugs can provoke tremor, including stimulants (e.g., theophylline, methylphenidate), dopamine receptor-blocking drugs, lithium, tricyclic antidepressants, anticonvulsants (e.g., valproate, phenytoin, carbamazepine), cardiac agents (e.g., amiodarone, calcium channel blockers, procainamide), and immunosuppressive agents (e.g., cyclosporin A, corticosteroids).

Front 85

DYSTONIA

Back 85

Dystonia consists of sustained muscle contractions that result in abnormal postures and contortions.

It may occur as a primary process or as a secondary symptom of an underlying neurologic disease (e.g., Wilson disease, Huntington disease, cerebral anoxia).

Derangements in the physiologic makeup of the dopamine synapse may lead to acute drug-induced dystonic reactions.

Such reactions can be life threatening if respiratory function is compromised, but they generally respond to emergent treatment with anticholinergic medication.

Metoclopramide (Reglan), commonly prescribed for nausea and vomiting, may induce dystonia.

DBS with implantable electrodes has been used experimentally for dystonia.

Front 86

WILSON DISEASE

Back 86

Wilson disease is a rare (approximately 1 per 40,000 births) but treatable autosomal recessive disorder that is debilitating and eventually fatal if left untreated.

It should be considered in the differential diagnosis of new-onset hyperkinesia or parkinsonism in the young adult.

Wilson disease almost never develops after the age of 50 years.

Wilson disease may also exhibit neuropsychiatric manifestations. Psychosis is common.

The disease is a systemic disorder of copper metabolism.

In addition to the neurologic signs and symptoms, hepatic dysfunction (including death from fulminant hepatic failure) occurs in variable degrees.

All young adult patients with a movement disorder should be screened for Wilson disease by means of a ceruloplasmin level.

In patients with suspected Wilson disease, slit-lamp examination for Kayser-Fleischer rings (i.e., characteristic depositions of copper pigment in the limbus of the iris), 24-hour urine collection for copper, determination of serum copper level, and hepatic biopsy are indicated.

Treatment with copper chelation and zinc can arrest further neurologic decline and can occasionally improve neurologic deficits.

Mobilization of copper from liver stores can result in neurologic worsening during initial treatment with standard chelation regimens.

Patients should be referred to experienced centers for initiation of treatment.

Front 87

HUNTINGTON DISEASE

Back 87

Huntington disease is an inexorably progressive autosomal dominant neurodegenerative disorder affecting motor function, cognition, and behavior.

The mean age at onset is 40 (10% of cases begin in childhood), and the mean duration of illness is 20 years.

In the adult-onset form, chorea affects the limbs and trunk.

Other movement abnormalities commonly occur, including dystonia, rigidity, postural instability, and myoclonus.

Bradykinesia and rigidity predominate in the juvenile-onset form.

Eye movements are often abnormal early in the disease, with slowing of saccadic initiation and velocity and eventual breakdown of smooth pursuit movements.

The disease involves premature death of specific neurons in the caudate and putamen.

Front 88

Physiologic (hypnagogic) myoclonus

Back 88

occurs in healthy individuals as they fall asleep.

Front 89

Essential myoclonus

Back 89

is a nonprogressive, generalized disorder that can occur as an autosomal dominant trait. Patients experience multifocal, large-amplitude lightning jerks that are provoked by action and are disabling, or they may have mild, small-amplitude jerks that do not disrupt their function. Patients with essential myoclonus almost always also have some degree of underlying dystonia.

Front 90

treatment of myoclonus

Back 90

Treatment should be directed to the underlying cause. Valproate or clonazepam are commonly prescribed for symptomatic treatment of myoclonus.

Front 91

TOURETTE DISORDER

Back 91

defined as the history of both motor and vocal tics (for more than 1 year) with onset before the age 18 years. The tics are associated with obsessions and compulsive behavior in 50% of patients and are accompanied by attention-deficit disorder in 50% of patients. Tourette disorder is probably an autosomal dominant condition with variable penetrance.

Front 92

Tourette disorder treatment

Back 92

Treatment focuses on the most functionally incapacitating aspect of the disorder (not necessarily the tics), and patients and families should be reassured that the disorder is not progressive or fatal.

Approximately two thirds of patients outgrow their tics (but not necessarily the other neuropsychiatric manifestations of the illness) by adulthood.

Useful medications are outlined in Table 122-10. Strategies to reduce stress on the patient, including education of parents, peers, and teachers, are frequently preferable.

Treatment of attention deficit with stimulants may exacerbate tics; treatment of tics with neuroleptic drugs may blunt affect, disrupt learning, provoke depression, and lead to unwanted weight gain.

Front 93

Medications Used in the Management of Incapacitating Tourette Disorder: TICS

Back 93

Neuroleptics (haloperidol, pimozide, others)
Clonidine (oral or transdermal patch)
Calcium channel blockers (diltiazem, verapamil)
Benzodiazepines (clonazepam, others)
Guanfacine

Front 94

Medications Used in the Management of Incapacitating Tourette Disorder: Obsessive-Compulsive Behavior

Back 94

Selective serotonin reuptake inhibitors (fluoxetine, sertraline, others)
Clomipramine

Front 95

Medications Used in the Management of Incapacitating Tourette Disorder:Attention-Deficit Disorder

Back 95

Stimulants (methylphenidate, pemoline)
Clonidine
Selegiline
Tricyclic antidepressants

Front 96

The cerebellum receives input from the

Back 96

spinal cord (spinocerebellar tracts), from the vestibular nuclei in the brainstem, and from pontine relays, carrying information from the motor and premotor cortex.

Front 97

The cerebellar cortex is made up of four main neuronal types.

Back 97

GRANULE CELLS input onto PURKINJE CELLS, whose axons form the sole output of the cerebellar cortex, terminating in cerebellar nuclei or select brainstem nuclei. GOLGI CELLS and STELLATE-BASKET CELLS function as inhibitory interneurons within the cerebellar cortex.

Front 98

The cerebellar cortex is organized into three main sagittal zones

Back 98

medial (vermal) zone

Front 99

cerebellar cortex sagittal zones: medial (vermal) zone

Back 99

projects to the fastigial nuclei, which in turn project to the vestibulospinal and reticulospinal tracts.

Injuries to this zone or its projections lead to abnormal stance and gait, truncal titubation, and disturbances of extraocular movement.

Front 100

cerebellar cortex sagittal zones: The intermediate (paravermal) zone

Back 100

projects to the interposed nuclei, which in turn project to the red nucleus and the thalamus.

Isolated injuries to this zone are rare, and clinical manifestations generally overlap with medial or lateral cerebellar syndromes.

Front 101

cerebellar cortex sagittal zones: The lateral zone

Back 101

projects to the dentate nuclei, which in turn project to the thalamus and cerebral cortex.

Injuries to this zone or its projections result in abnormal stance and gait, appendicular dysmetria, eye movement dysmetria, dysdiadochokinesia, dysrhythmokinesia, intention tremor, ataxic dysarthria, and hypotonia.

Front 102

Lesions of the cerebellum, its inflow tracts, or its outflow tracts may all be associated with

Back 102

ataxia

Front 103

The rapid onset of ataxia suggests an

Back 103

underlying structural condition, an immune-mediated process, drug intoxication, or conversion disorder.

Radiographic studies, drug screening, and cerebrospinal fluid analysis will clarify the diagnosis in most patients with acute-onset ataxia.

Front 104

Chronic or progressive ataxia may result from

Back 104

slow-growing brain tumors (e.g., cerebellar astrocytoma, hemangioblastoma, ependymoma, medulloblastoma, supratentorial tumors), congenital malformations (e.g., basilar impression, Dandy-Walker malformation, Chiari malformation), drug effects (e.g., alcoholic cerebellar vermian degeneration, chronic phenytoin toxicity), or hereditary ataxias.