Neuro Lect 8
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Central processing center with roles in movement, cognition, emotions and learning.
What are the feedback loops and neurotransmitters involved with the basal ganglia?
- positive/negative control
- dopamine, glutamate, GABA
A rhythmic oscillatory movement characterized by its relationship to voluntary motor activity and is often enhanced by emotional stress and disappears during sleep. Is relieved with medications and alcohol.
Type of tremor that is sometimes to referred to as a benign tremor and is the most common. Is mild and non progressive in some people, and in others is slowly progressive starting on one side of the body and spreads to effect both sides within 3 years. Hands are most often affected but the head (yes-yes/no-no motion), voice, tongue, legs and trunk can also be involved causing mild gait disturbances. Frequency may decrease as a person ages but severity may increase, affecting the person's ability to perform certain tasks or activities of daily living. Affected by emotion, stress, fever, physical exhaustion/low blood sugar but is not associated with any known pathology.
Type of tremor caused by damage to structures within the brain that control movement. Causes a resting tremor which can occur as an isolated symptom or be seen in other disorders. Is classically seen as a "pill-rolling" action of the hands that may also affect the chin, lips, legs and trunk and is markedly increased by stress or emotions. Onset is generally after age 60 with movement starting in one limb or one side of the body that progresses to include the other side.
Type of tremor that occurs in individuals of all ages who are affected by a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions and/or painful and abnormal postures or positions. 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 tremor may differ from essential tremor by occurring irregularly and obtaining relief with complete rest. Touching the affect body part or muscle by reduce the severity.
Type of tremor that is a slow, broad tremor of the extremities that occurs at the end of a purposeful movement, such as trying to press a button or touching a finger to tip of one's nose. Is caused by lesions or damage to the cerebellum from stroke, tumor or disease such as MS or inherited disorders. Also occurs due to chronic alcoholism or overuse of some medications.
The classic presentation of this type of tremor occurs with a lesion to one side of the brain which produces a tremor on that same side of the body which worsens with directed movement. Can also produce a "wing-beating" type of tremor called rural or Holmes tremor (combination of rest, action and postural). Tremor is most often prominent when person is active or maintaining a particular posture.
Type of tremor that can occur at rest or during postural or kinetic movement. The characteristics vary but generally include sudden onset and remission, increased incidence with stress, change in tremor direction and/or body part affected and greatly decrease/disappear when the patient is distracted. Many patients with this type of tremor have a conversion disorder or other psychiatric disease.
psychogenic tremor (aka hysterical tremor)
Type of tremor characterized by rhythmic muscle contractions that occur in the legs and trunk immediately after standing. Cramps are felt in the thighs and legs and patient shakes 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. This tremor may also occur in patients who have essential tremor.
Type of tremor that occurs in every normal individual and has no clinical significance. Is rarely visible to the eye and may be heightened by strong emotion (anxiety/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 one of the hands. The enhanced form of this tremor is strengthening to a more visible level. It is generally not caused by neurologic disease and is usually never visible once the underlying cause is corrected.
Involuntary, arrhythmic, rapid, purposeless movements. Patients have difficulty maintaining muscular contraction for strength testing. Speech becomes irregular. Disappears during sleep.
chorea (greek word for "dance")
What are the characteristic deficits in strength testing in a patient with chorea?
- hand grip may relax intermittently (milkmaid grasp)
- gait is irregular and unsteady; pt suddenly dips or lurches to one side or the other (dancing gait)
- speech is irregular in volume and tempo; may be explosive in character
Pathophysiology for this condition is not definitive but is associated with cell loss in the caudate nucleus and putamen and can be provoked by dopaminergic agonist drugs.
- Note: if it is due to a treatable disorder the treatment will abolish the dyskinesia
What are hereditary causes for chorea?
- wilson's disease
- benign hereditary chorea
- dentatorubro-pallidoluysian atrophy
What are the cerebral vascular disorders that can cause chorea?
- subdural hematoma
Neurological disorder of childhood resulting from infection via GABHS that is characterized by rapid, irregular and aimless involuntary movements of the arms and legs, trunk and facial muscles.
- sydenham's chorea
- Note: affects girls more than boys, typically occurs between 5-15 yrs of age
What is the treatment for sydenham's chorea?
- mildest form: bed rest during period of active movements is sufficient
- severity interfering with rest: sedative drugs (barbituates/benzos), or anti epileptic meds (valproic acid)
A rare maternal complication during pregnancy that shows extrapyramidal symptoms with involuntary movements, lack of coordination, slurred speech and psychic disorders. Neurological state is normal except for a lost of muscle tone.
When do the symptoms of chorea gravidarum usually manifest? When does it typically resolve?
- first trimester (one case study shows chorea beginning in the 9th week)
- spontaneously resolves after 2-3 months
What is the treatment for chorea gravidarum in which subjectively disturbing symptoms manifest?
- anticonvulsive and sedative therapy with benzos or neuroleptics
- elective termination of pregnancy is not indicated
What are the different categories of chorea?
- hereditary: huntington's, wilson's, benign hereditary chorea
- sydenham's chorea: acute rheumatic fever
- chorea gravidarum
- drug toxicity: OCPs, lithium, etc
- cerebral vascular disorders: vasculitis, subdural hematoma, stroke
A unilateral chorea that is especially violent (wild, flail-like movements) involving proximal muscles of limbs like the shoulder. Is most often due to vascular disease in the contralateral sub thalamic nucleus.
- Note: it is the most dramatic movement disorder seen in clinical practice
What is the etiology for hemiballismus?
- any focal process but the elderly generally get it due to vascular events or nonketotic hyperglycemia
- infectious or inflammatory processes are more common in younger patients
How is hemiballismus generally treated?
- dopamine receptor blocking agents: first line for acute treatment
- neuroleptics: haloperidol, perphenazine (started low and titrated until movements are controlled)
- atypical antipsychotics: risperidone, clozapine (reduce extrapyramidal side effects)
- catecholamine depleting agents: reserpine, tetrabenazine (long term therapy)
- sterotactic functional neurosurgery: when movements persist
Slow, sinuous, writhing involuntary movements (i.e. flexion, extension, pronton, supination of fingers and hands) that disappear during sleep. Is frequently seen in association with symptoms of cerebral palsy.
- Note: when held as a prolonged posture it is considered dystonia
The first signs of athetosis may be apparent as early as 18 months from birth. What are usually the first signs?
- difficulty feeding
- poor sitting balance
- hearing loss
- speech impairment
- uncontrolled movements of the face, hands and feet which aggravates with time through adolescence and sometimes emotional stress
What is the cause of athetosis?
lesions in the corpus striatum, hippocampi and thalamus
What is the treatment for athetosis?
- medications to manage jerky involuntary movements: levodopa/diazepam (high dose)
- muscle training: helps pt get better control affected limbs
- psychological counseling: tackles stress, anxiety and excitement if they are regular triggers
- surgery: comes with risks such as limb paralysis
Sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures that are absent during sleep and enhanced by voluntary activity.
- Note: movements may be painful, and some pts may have a tremor or other neurologic features
What are examples of focal dystonia?
- writer's cramp
What are examples of generalized dystonia?
- cerebral palsy
- acute dystonic reactions
Difficulty or slowness in performing voluntary movements as well as involuntary movements of the face/tongue. May develop after long term treatment with antipsychotic drugs (dopamine receptor blockers) or with metoclopramide (reglan).
What are the clinical features of tardive dyskinesia?
- tongue protrusion
- lip smacking
- puckering and pursing
- rapid eye blinking
- rapid movements of arms, legs and trunk
What is the treatment for tardive dyskinesia?
- stop or minimize the neuroleptic drug
- replacing the drug with a substitute may also help some patients
- the only approved drug treatment is tetrabanzine
- benzos, clozapine or botulinum toxin injections may also be tried
What is the prognosis for tardive dyskinesia?
- symptoms stop spontaneously in most cases
- may persist indefinitely in others
Sudden, rapid, twitch like muscle contractions that may be spontaneous or brought on by sensory stimulation, arousal, or initiation ov movement. Classified according to distribution, relationship to precipitating stimuli, or etiology.
What are the classifications of myoclonus?
- generalized: widespread
- focal/segmental: restricted to particular part of the body, can arise from lesions affecting the cerebral cortex, brainstem or spinal cord
What is the treatment for myoclonus?
- anticonvulsants: valproic acid, barbiturates, phenytoin, primidone
- benzos: clonazepam (drug of first choice)
What are the four types of myoclonus?
- physiologic myoclonus: "nocturnal myoclonus" (twitches may awaken pt from sleep), hiccups
- epileptic myoclonus: associated with some seizures
- pathologic myoclonus: movements brought on by epilepsy or head injury, stroke, etc
- asterixis: hepatic encephalopathy
- Note: physiologic myoclonus occurs in healthy people, essential myoclonus is an isolated abnormality, symptomatic myoclonus occurs as a feature of a variety of degenerative, infectious or metabolic disorders
Sudden recurrent, quick, coordinated movements of motor or phonic muscles that can be either simple or complex.
What is the difference between motor and phonic tics?
- motor: affect discrete muscle groups
- phonic: involuntary sounds produced by moving air through the nose, mouth or throat
What is the difference between simple and complex tics?
- simple: sudden, brief, meaningless movements (blinking)
- complex: more purposeful and longer duration (touching clothes/people)
What are some examples of simple phonic tics?
What is an example of complex phonic tics?
- Tourette's syndrome
- repeating sounds/words
Neurological disorder characterized by repetitive, stereotyped, involuntary movements and vocalizations typically noticed first in childhood with the average onset between the ages of 3 and 9 years old.
What are things that can worsen and improve tourette's symptoms?
- worse: stress
- improved: concentration
- Note: suppressing the movement may cause great anxiety, tics disappear during sleep
How is the cause of abnormal movements identified by the age of onset?
- present since infancy: cerebral palsy or kernicterus
- developed in childhood: likely to be tics
- early in adult life: benign essential tremor, Huntington's disease
- elderly: parkinson's disease
How is the cause of abnormal movements identified by the mode of onset and clinical course?
- abrupt onset in child or young adult: drug-induced reaction
- gradual onset of dystonic postures and movement: chronic disorders (i.e. wilson's dz)
- abrupt onset of chorea or ballismus in adult: suggests vascular event
- gradual, insidious onset and progression: suggests degenerative process
What are the drugs that report "tardive dyskinesia" or "extrapyramidal symptoms" as an adverse reaction?
- reglan (anit-emetic)
- phenergan (anti-emetic)
- haldol (anti-psychotic)
What are the selected few hereditary causes of movement disorders of main concern?
- essential tremor
- tourette's syndrome
- huntington's disease
- wilsons disease
What are some specific common movement disorders?
- familial/benign essential tremor
- restless leg syndrome
- acute dystonia
- parkinson's disease
- huntington's disease
What is the gene mutation that is associated with causing 50% of essential tremor cases? What does the mutation do?
- ETM1, ETM2 (autosomal dominant)
- affects dopamine receptors
- Note: the remaining 50% of cases are idiopathic
How is essential tremor diagnosed and when is the typically onset of disease?
- clinical dx (rhythmic tremor 4-12hz present only when muscle is exerting effort)
- onset is from birth to senility
What are four things that make essential tremor worse?
What areas of the body are usually affected the most by essential tremor?
- *legs, head voice, tongue less frequently*
What is the drug treatment for essential tremor?
- propranolol 40mg po BID (most common)
- also decreases with a "small quantity of alcohol" but may lead to dependence/abuse
What is the treatment for severe cases of essential tremor?
high-frequency thalamic stimulation or surgery
Sudden onset of sustained muscle contraction, frequently causing twisting and repetitive movements or abnormal postures. Pathophysiologic basis of disturbance is unclear.
What are the differential diagnoses of acute dystonia?
- black widow spider bite
What are the antipsychotic/neuroleptic drugs (dopamine receptor blockers) that may be associated with acute dystonic reactions?
- phenothiazines: chlorpromazine (thorazine), fluphenzaine (prolixin)
- haloperidol (haldol)
- atypicals: olanzapine (zyprexa), resperidone (risperdal)
What are the phenothiazine anti-emetic drugs that may be associated with acute dystonic reactions?
- promethazine (phenergan)
- prochlorperizine (compazine)
What drugs besides antipsychotics/neuroleptics and phenothiazine anti-emetics may be associated with acute dystonic reactions?
- cocaine, LSD
- tricyclic antidepressants (amitriptyline)
- anticonvulsants (phenytoin, carbamazepine)
What are the patterns of drug-induces acute dystonia?
- laryngeal dystonia: dysphagia, stridor, "hot cup of tea sign"
- oculogyric crisis: involuntary deviation of the eyes due to contraction of extra ocular muscles
- buccolingual crisis: forced spasm of the face, jaw, tongue
- opisthotonus: forced spasm of the paravertebral muscles, forcing the trunk and neck into hyperextension
What is the emergency management of acute dystonia focused on?
- discontinuing offending drug
- administrating an anticholinergic drug
- admission to ICU is there is evidence of airway involvement (dysphagia, dyspnea, dysphonia or stridor)
What are the drugs used to treat acute dystonia?
- benztropine (cogentin) 1-2mg IV over 2 mins
- diphenhydramine (benadryl) 50-100mg IV over 2 mins
- Note: doses for each may be repeated after 15-30 minutes if symptoms persist, also use the same dose po TID for 2-5 days after resolution of symptoms to prevent relapse
What does failure of acute dystonia to respond to repeated doses of an anticholinergic drug indicate?
- non-drug induced dystonia
- disease mimicking an acute dystonic reaction
An "involuntary" movement disorder first described in the 17th century by Theodor Wittmack as an urge to move the limbs with/without sensations that worsens with relaxation (esp at night) and improves with activity.
restless leg syndrome
What are the sensations of restless leg syndrome described by affected individuals?
- range in severity from uncomfortable to irritating to painful
What are the causes of restless leg syndrome?
- medications (TCAs, SSRIs)
- opiate withdrawal
- pregnancy (can worsen it)
What conditions are associated with restless leg syndrome?
- iron deficiency anemia
- folate deficiency
- sjogren's disease
- celiac disease
- rheumatoid arthritis
- varicose veins
- thyroid disease
What is the treatment for restless leg syndrome?
- benzos: clonazepam
- dopamine agonists: levodopa, pramipexole (mirapex) 0.125-0.5mg po qpm, ropinirole (requip) 1-2mg po qpm
- anticonvulsants: gabapentin
What are the clinically defining characteristics of parkinson's disease?
- resting tremor
- cogwheel rigidity
- impairment of postural reflexes
Progressive neurological disorder affect 1% of the population over 60 yrs and is characterized by cytoplasmic eosinophilic inclusions (lewy bodies) in neurons of the substantia nigra and locus ceruleus and by depigmentation of the brain stem nuclei.
In parkinson's disease, damage in the substantia nigra occurs with cell loss in the basal ganglia which leads to the movement disorder/impaired motor function. Why is dopamine important in this disease process?
- it exerts an inhibitory effect on release of GABA
- GABA output increases without dopamine which causes an imbalance between GABA and ACh levels
What does the acronym TRAP mean in regards to the presenting symptoms of parkinson's disease?
- Tremor: resting tremor
- Rigidity: may complain of muscle stiffness
- Akinesia/bradykinesia: slowing of fine movements, reduced speech volume, slowed speed when dressing and eating
- Postural instability: walking becomes slower ("festinating gait"), difficulties with turning ("en bloc"), difficulty rising from chair
The tremor from what disease disappears with purposeful movements of the hands and eventually causes lost facial expressiveness and drooling?
What are the late features of parkinson's disease?
- orthostatic instability
- motor complications (freezing, on-off, dyskinesias)
- whole body movement abnormalities
- dementia (frontal lobe dysfunction)
- dysautonomia (MSA, striatonigral degeneration)
- skin greasiness/seborrhea on forehead, face
A late complication of levodopa therapy which there is a fluctuation in response to the drug caused by a deterioration just shortly before the next dose is taken. Is abrupt but transient and may occur at frequent intervals during the day without respect to dose or dose timing (is sometimes disabling).
- parkinson's OFF ON OFF phenomenon
- Note: may be controlled by varying dosing intervals 1 hour before meals, restricting dietary protein, and using dopamine agonists like carbadopa
When is levodopa therapy in conjunction with carbadopa contraindicated?
- pts with narrow angle glaucoma
- pts with psychotic illness
- pts with active peptic ulcer disease
- pts with suspected malignant melanoma
What pattern shown on a PET scan corresponds with a diagnosis of parkinson's disease?
- decreased dopamine activity in the basal ganglia
- Note: diagnosis itself is on a clinical basis only
What is the most effective treatment for bradykinesia and rigidity caused by parkinson's disease?
dopamine replacement: carbidopa/levodopa (sinemet) 800mg po qd
What medications help with the rigidity and tremor caused by parkinson's disease?
anticholinergics: benztropine (cogentin) 1-6mg po qd
What medications are best for young patients with mild parkinson's disease?
dopamine agonists: bromocriptine (parlodel) 10mg po TID (stimulates dopamine receptors)
What medication augments dopamingeric activity and is used in patients with mild parkinson's disease?
amantadine (symmetrel) 100mg po BID
What medications are used as neuroprotection for patients with mild parkinson's disease?
- selegeline (MAO-B inhibitor) 10mg qam: inhibits enzymes that break down dopamine
- coenzyme Q10: enhances mitochondrial function
What is the prognosis for patients with parkinson's disease?
- majority of pts show lessening response to medical therapy in 5 years of treatment
- various movement disorders develop as a result of long-time therapy (dyskinesia, dystonic postures)
- there to no medical therapy that reverses or cures the disease
- death often occurs from choking, pneumonia or falling
- progression may take 20 years or more
What are the surgical procedures that can be performed on patients with parkinson's disease once they are unresponsive to medical therapy?
- Note: deep brain stimulation of the sub thalamic nucleus can improve parkinson's disease symptoms
What is the physical therapy used to help treat pts with parkinson's disease?
- retraining walking and transfer techniques
- Note: maintaining max activity is the goal of PT
Why is speech therapy used to treat pts with parkinson's disease?
improves speech and swallowing technique
Gradual onset of involuntary movements, changes in behavior, personality, and cognitive impairment with symptoms taking years to develop fully leaving the patient as a "quivering wreck of his former self".
What is the pathophysiology of huntington's disease?
- genetic mutation causes premature cell death resulting in atrophy of the cerebral cortex and caudate
- concentrations of GABA and ACh in the basal ganglia are reduces with increased levels of dopamine
- transmitted as an autosomal dominant gene with usual onset at 30-40 yrs of age
What are the signs and symptoms of dementia associated with huntington's disease?
- early: irritability, moodiness, antisocial behavior
- later: early symptoms followed by progressive dementia
What are the signs and symptoms of chorea associated with huntington's disease?
- may seem like restlessness at first
- progressive in severity
- affects all limbs along with central involvement
- patient cannot maintain tongue of a protruded position (tongue protrusion test)
What does CT or MRI imaging show in a patient with huntington's disease?
atrophy of the cerebral cortex as well as caudate nucleus (helps differentiate from AD)
What is the medical treatment for huntington's disease?
- haloperidol: helps with movements
- reserpine: thought to deplete dopamine from receptor terminals
- SSRIs (prozac): helps with moodiness and aggressiveness
- benzos: helps with sleep and anxiety
Drug approved for treating chorea in huntington's disease on 15 Aug 2008 that works by reversibly inhibiting vesicular monoamine transporter 2 making it a centrally acting, dopamine depleting drug.
- xenazine (tetrabenazine)
- Note: significantly reduces chorea burden and is generally safe and well tolerated, but can slightly worsen mood, cognition, rigidity and functional capacity
What are the side effects of xenazine (tetrabenazine)?
What is the prognosis for patients with huntington's disease?
- no cure
- progressive dementia
- life expectancy of 10-25 years after onset of symptoms
- death usually due to infection (pneumonia) or fall related injuries
- patients have higher than average suicide rate
Presence of illness behavior based on a wish to be a patient and experience the sick role with no other apparent motivators.
- factitious disorder
- Note: munchausen's syndrome is the most extreme
Faking symptoms based on external incentive (avoid work, incarceration, get insurance money), patient may actually reveal these goals.
What are examples of consciously invented symptoms?
- factitious disorder
What are examples of unconsciously produced symptoms?
- somatization disorder
- undifferentiated somatoform disorder
- conversion disorder
- pain disorder
- body dysmorphic disorder
- somatoform not otherwise specified
Unexplained physical symptoms manifested before age 30 that last for several years and include two GI, four pain, one pseudoneurologic and one sexual.
- somatization disorder
- Note: >/= six month history with one or more unexplained physical symptoms is undifferentiated somatoform disorder
Somatoform disorder with a single unexplained symptom involving voluntary or sensory functioning.
Somatoform disorder in which a pain symptom is the predominant focus with psychological factors that play the primary role in the perception, onset, severity, exacerbation or maintenance of pain.
Somatoform disorder involving a fixation on the fear of having a life threatening medical condition.
Somatoform disorder involving preoccupation with a real or imagined physical defect.
body dysmorphic disorder
Somatoform disorder in which there is a misinterpretation or exaggeration of unexplained physical symptoms.
- somatoform not otherwise specified
- Note: pt does not meet full criteria for any of the other somatoform disorders
Why do somatiform patients tend to go to PCP offices and ERs?
- lack of insight into psychiatric illness
- seldom present to psychiatric clinics
- stigma associated with psychiatrists
The tendency to experience psychological distress in the form of somatic symptoms and seek medical help that may be influenced by the desire for personal gain.
somatization disorder (UNCONSCIOUS!)
What symptoms are needed to diagnose a somatization disorder?
- 2 GI
- 4 pain
- 1 neuro
- 1 sexual
Excess preoccupation with symptoms due to fear of having a serious disease based on misinterpretation of normal bodily functions.
- Note: prevalence is up to 7% in the primary care outpatient setting (men=women)
Symptoms of voluntary motor or sensory function dysfunction that suggests a neurologic or other medical disease but cannot be explained. Single episodes are usually short but may be prolonged if secondary gain is involved (not obvious).
- conversion disorder
- Note: pt UNINTENTIONALLY develops symptoms or deficits affecting voluntary motor or sensory function to suggest a neurologic or other medical condition
What are some examples of conversion disorder?
- paralysis of extremity
- complaints of blindness
- sensory complaints that do not follow neurologic parameters
- Note: is usually seen in pts with little formal education and low socioeconomic status, also may be more common among military personnel
What are some coexisting psychiatric disorders that accompany somatoform disorders?
- substance abuse
- depression (greater than half the pts with MDD present with only somatic symptoms)
- anxiety (panic attacks are accompanied by a variety of somatic symptoms)
- personality disorders (BPD)
What are clues pointing to a diagnosis of pseudoneurologic syndromes?
- precipitated by stress
- occurs or worsens in the presence of others
- signs of other psychiatric illness
- histrionic personality
- history of multiple surgeries, hospitalizations, and ER visits
- no serious injuries
- denies psychological etiology of symptoms
- symptoms persist despite specific treatment
- vague, bizarre, inconsistent description of symptoms
- inconsistencies on repeated exams
- non-anatomic distribution of complaints
Difficult to distinguish from actual epileptic seizures, but are prevalent and may coexist with epileptic seizures. Patients are usually female with onset in their late teens. History of sexual abuse or trauma is common. May be an expression of rage, fear, and helplessness.
- Note: are similar to "temper tantrum" of a young child, health related traumatic events are more likely to incite this in older patients (may need to do a video EEG)
What are the historical features that suggest pseudo seizures?
- high seizure frequency
- emotional or situational trigger
- gradual onset and cessation
- patient is able to recall precisely what occurred during the seizure
- no response to anti epileptic drugs
- personal, family, or professional experience with epilepsy
What are the clinical clues used to identify pseudo seizures?
- no lateral tongue biting
- no post-ictal confusion
- no injuries related to "seizures"
- dystonic posturing
- asynchronous limb movements
- pelvic thrusting during seizures
- geotropic eye movements
- closed eyes during seizures
- corneal reflex intact
- side to side head movements
- ictal crying, weeping
- intermittent or waxing and waning motor activity
- prolonged seizures (2-3 minutes)
- may be terminated by painful stimuli
- normal ictal EEG
- normal serum prolactin level
Patient reports involvement of a single limb or one half of the body as being paralyzed with weakness that does not follow anatomic patterns.
What are the clinical clues that suggest pseudoparalysis?
- weakness does not follow anatomic patterns
- normal reflexes, negative Babinski, normal muscle tone and sphincter function
- face, tongue, SCM not usually affected
- weakness is inconsistent
- "give way" weakness
- drop test (arm will not strike pts face)
- hoover test (counter pressure is felt when pt lifts leg against resistance)
- adductor sign (weak side will contract normally when patient adducts "good" leg)
- "hysterical gaits" present
Patients complain of numbness and tingling that follow the patient's own concept of anatomy. Is common to see hemisensory loss with nonphysciologic midline sensory split with this condition (i.e. genitals, hearing, vision, smell, taste=overlapping innervation).
What are the clinical clues that suggest pseudo sensory syndrome?
- painful stimuli may result in withdrawal of the "numb" extremity
- vibratory loss over one half of the "numb" sternum, pelvis, or skull (physiologically impossible due to bone conduction)
- bowles and currier test (pt with true impairment can identify fingers with normal and abnormal sensation with sharp stimulus, pseudo pts make mistakes identifying the "numb" fingers)
- yes-no sensory test (have pt close eyes and touch limbs, a repeated "no" on a "numb" limb suggests pseudo sensory)
- proprioception (100% abnormal), pts with true organic lesions have 50/50 chance of being correct
What is used to identify nonorganic causes of back pain?
What are the Waddell signs?
- superficial tenderness: skin discomfort on light palp
- nonanatomic tenderness: crosses multiple anatomic boundaries
- axial loading: pain elicited by pressing down on pts head
- pain on simulated rotation: rotating shoulders and pelvis together should not be painful
- distracted straight leg raise: if pt complains of pain on straight leg raise but not if the examiner extends the knee with the pt seated
- regional sensory change: stocking sensory loss or sensory loss in an entire extremity/side of body
- regional weakness: jerky with intermittent resistance (cogwheel/catching), organic weakness can be overpowered smoothly
- overreaction: exaggerated painful response to stimulus that is not reproduced when same stimulus is given later
Should be a diagnosis of exclusion that usually begins with an observer present. Patient "slumps" to the floor to avoid hitting their head.
What are the clinical clues that suggest pseudocoma?
- pt resists exam and makes avoiding movements
- keeps eyes closed tightly, resists attempts to open them
- eyes divert upward when lids are opened
- pts respond with purposeful movement to painful stimuli and to avoid unpleasant stimuli
- pts hand will "just miss" when dropped towards face
- caloric testing results in nystagmus, nausea and/or vomiting
- "comatose" period should be used to obtain blood and urine samples
What are the psychogenic movement disorders?
- pseudotremor: abrupt onset, intentional, disappears with distraction
- psychogenic parkinsonism: "hysterical gaits"
- psychogenic myoclonus: periods of spontaneous remission
- psychogenic dystonia: abrupt onset, inconsistent exam
Sudden "blindness" that involves complete loss of vision with diplopia as a common complaint.
What are the clinical clues that suggest pseudoneuro-ophthalmologic syndrome?
- normal pupillary response & optic fund exam excludes all organic causes except cortical blindness
- cortical blindness is excluded by normal optokinetic nystagmus or response to a mirror in front of a patient
- normal fundoscopic exam excludes monocular diplopia (but suspect nonorganic cause)
What are the practice management strategies for somatoform disorders?
- most conversion symptoms are transient and respond to supportive treatment
- recognize that the patient's problems are important to them
- explain they do NOT have a serious physical problem and reassure them that no significant deterioration in condition is expected
- tell them that exercise may be uncomfortable but will not negatively affect their condition
- you may have to tell patients who overtly exhibit malingering that you cannot help them
- directly confronting patients who are psychologically invested in their pain is generally UNWISE
- psychologically disturbed pts should be referred to a psychotherapist
What are conversion disorders also known as?
What would you like to do?
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