Examinarea neurologica

The Neurologic Examination: Sensory System

 Introduction
Cranial Nerves
Motor Exam
Inspection and Palpation
Reflexes
Gait
Sensory System
Reading List
Introduction
The basic neurologic examination includes six primary components -- examinations of the patient's:

Mental status
Cranial nerves
Coordination
Sensation
Motor system
Gait
When performing a neurologic examination on a patient with a movement disorder or who is suspected to have a movement disorder, the primary findings will, obviously, be apparent when examining the motor system. However, many other aspects of the neurologic exam may be abnormal as well. This review is intended to highlight the basic examination with an emphasis on those areas that are of particular interest, as they pertain to patients with movement disorders or who are suspected to have a movement disorder.

Mental Status
When conducting an assessment of mental status, it is important to keep in mind that many factors may have an impact on the results of the patient's exam. Some factors include the time of day during which the exam is conducted; the patient's levels of stress, fatigue, pain, and education; and the patient's socioeconomic status. The mental status exam includes ascertainment of the levels of consciousness (i.e., normal, depressed, or hyper-alert), attention, and cooperation. A brief assessment of cognitive functioning identifies deficiencies in orientation, the patient's fund of knowledge, memory, insight and judgment, concentration, ability to perform calculations, abstract thought, and verbal fluency.

Generalized impaired attention and cooperation are nonspecific findings and not likely to be related to a movement disorder. If difficulties in language and calculations are present, identifying these may help to specify the location of any underlying lesions. Movement disorders in which cognitive impairment is a prominent finding include:

Lewy body disease
Corticobasal degeneration
Late-stage Parkinson's disease
Huntington disease
A very small percentage of patients with late-stage Wilson's disease may show evidence of cognitive impairment as well.

Key point/callout: Pain, stress, low levels of education, and the cognitive impairment that may manifest during late-stage Parkinson's disease may all inhibit a patient's ability to attend to and process new information and recall previously stored information.

Cranial Nerves

Careful assessment of cranial nerves can assist the clinician in identifying specific neurologic lesions or deficits that are related to movement disorders. Assessing olfaction (cranial nerve I) is particularly important in differentiating Parkinson's disease from other parkinsonian syndromes. In Parkinson's disease, pupillary reflex imbalance (cranial nerves II and III) may occur, primarily through involvement of the parasympathetic system.

Disorders of eye movements usually manifest as instability of visual gaze (nystagmus -- periodic, rhythmic ocular oscillation involving vertical, horizontal, and/or torsion movements) or jerkiness of pursuits (eye tracking) or saccades (visual scanning) (cranial nerves III-V). Periodic nystagmus is often found in patients with spinocerebellar degeneration, and pendular nystagmus in those with brain stem or cerebellar degeneration, including patients with Parkinson's disease.

By definition, opsoclonus-myoclonus involves irregular, rapid eye movements. Abnormalities in eye movements are also often seen early in the course of Huntington disease. These abnormalities are primarily related to saccades, as evidenced by slow initiation, lack of coordination, intrusion into and disruption of smooth pursuit, and lack of inhibition in response to a peripheral stimulus when attempting to look in the opposite direction.

The hallmark of progressive supranuclear palsy (PSP) is a down-gaze palsy in which the patient is unable to look down on command even though, when the examiner lifts the patient's head, the patient is able to track downward. Other difficulties with eye movements that are common in patients with PSP include impaired saccades, slow visual pursuit, unstable fixation, and disturbed convergence. Manifesting as blurred vision, double vision, or reading difficulty, these visual impairments may worsen the gait and balance problems found in patients with progressive supranuclear palsy. (See video examples of disordered eye movements)

Several forms of dystonia may have abnormal findings on examination of the cranial nerves.

Blepharospasm is posited to involve abnormal plasticity of the neuronal circuits mediating blink reflexes (V and VII). Dysfunction of cerebellar afferent pathways may underlie the pathophysiology of cervical dystonia, with potential involvement of the 11th cranial nerve.

Hemifacial spasm, a form of segmental myoclonus, is characterized by involuntary, paroxysmal, tonic, or clonic contractions of the muscles innervated by the seventh cranial nerve. Cranial nerves V, VII, IX, X, and XII are involved in the articulation of speech. Abnormalities in one or more of these nerves may be manifest in spasmodic dysphonia and the hypophonia of Parkinson's disease.

Key point/callout: Nystagmus is an eye movement disorder that manifests as an instability of visual gaze with periodic, rhythmic ocular oscillation involving vertical, horizontal, or torsion movements or a combination thereof.

Key point/callout: Abnormalities of eye movement are common in patients with Huntington disease, with an increase in saccade latency and a higher variability in saccade latency.

Motor Exam

Examination of the motor system involves observation, palpation, and assessment of tone, function, and strength. The first step in the examination of the motor system is to simply observe the patient.

Observation

Abnormal Movements

If spontaneous, abnormal, adventitious movements -- not an abnormality of normal movements -- are found, they should be characterized according to type, age of the patient at onset, mode of onset, and clinical course of the movements. Abnormal hyperkinetic movements include tremor, tics, dystonia, chorea, ballismus, myoclonus, and athetosis, all of which usually decrease in intensity and frequency or disappear during sleep. Factors related to the temporal onset of hyperkinetic movements and recent institution of dietary, pharmacologic, or homeopathic remedies, including recent or long-term exposure to toxins, should be noted. Time of day when the movements occur most commonly must be also be identified.

Tremor

Tremor, an involuntary, rhythmic oscillatory movement of one or more parts of the body, results from alternating or irregularly synchronous contractions of antagonist muscles. Tremor can be differentiated according to:

  • The involved body part
  • Provocative and palliative factors
  • Frequency (i.e., fast versus slow) of the movement
  • Amplitude (i.e., coarse versus fine) of the movement

When assessing tremor, it may be helpful to observe patients with their hands resting in their laps and while writing or drinking, to have them draw (such as an Archimedean spiral), and to perform the finger-nose-finger test.

Tremor type. The subsequent exam should further delineate the tremor type. An action tremor is usually exhibited when the body part is moved from one point to another (kinetic tremor), with muscle contraction against a fixed object (isometric tremor), and or when writing or performing other specific activities (task-specific tremor). The typical frequency of an action tremor is between 3 and 10 Hz.

A postural tremor is exhibited when the position of the body part is maintained against gravity. To elicit this type of tremor, the clinician can simply ask the patient to extend his or her arm or leg, as indicated, and hold it in that position for a period of time. Essential tremor, the most common type of postural tremor, has a moderate to high frequency and low amplitude.

A rest tremor, by definition, is exhibited while the affected body part is at rest. The tremor is typically worse during mental distraction, i.e., during the cognitive assessment while the patient is counting by 7's. A rest tremor decreases with intentional movement, has a low to moderate frequency (i.e., 3-6 Hz), and has a high amplitude. The tremor of Parkinson's disease is an example of a rest tremor, although this may also be a mixed tremor, and 20% of patients with Parkinson's disease have no tremor at the onset of disease.

Tics

Because these unvoluntary (as opposed to involuntary in that the movements can often be suppressed, albeit with a resultant increased level of patient discomfort), compulsive, repetitive, stereotyped movements may not always be readily apparent or observable during the neurologic examination, obtaining a valid history or reviewing videotape of the tics may be necessary. Tics may be motor or vocal, or a patient may have both motor and vocal tics. The tics should be classified as simple or complex.

Simple motor tics are typically abrupt, brief, repetitive isolated movements, such as eye blinking or facial twitching, neck stretching, head jerking, or shoulder shrugging.

Complex motor tics involve several muscle groups and may be manifest as repetitive squatting, skipping, hopping, or even more complex movements (see the table below).

Manifestation of Complex Motor Tics
Touching of others
Deep knee bending
Jumping
Smelling of objects
Hand gesturing
Head shaking
Leg kicking
Turning in a circle

Simple vocal tics include grunting, throat clearing, sighing, barking, hissing, sniffing, tongue clicking, or snorting, with complex vocal tics involving phrases or words.

During the examination, other factors should be elicited related to the tics, including the frequency of occurrence and suppressibility of the tics, as well as any provocative factors related to the tics.

Dystonia

Dystonia is characterized by sustained muscle contractions that frequently cause twisting or repetitive movements and abnormal, sometimes painful, postures or positions. Dystonia may affect any part of the body, including the arms, legs, trunk, neck, head, or face. The examiner should note the involved body part or parts, provocative factors, and sensory "tricks" that the patient may employ to suppress the movement.

Key point: dystonia: is a neurologic movement disorder characterized by sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions. Almost all dystonic movements share a directional quality that is typically sustained, sometimes for an instant, as well as a consistency and predictability. Dystonic movements are directional, forcing the involved body part or region into an abnormal position, which is consistently present.

Chorea

The involuntary, rapid, irregular, jerky movements of chorea may affect one or more parts of the body, including the face, arms, legs, or trunk. The two most commonly encountered disorders with choreiform movements as a primary component are Huntington disease and Sydenham chorea. The examination should include delineation of the involved body part.

Athetosis. The involuntary, relatively slow, writhing movements of athetosis are often found in combination with other abnormal movements, such as chorea. The examination should include notation of affected body parts, which typically include the face, neck, tongue, and hands, but may affect any muscle group.

Choreiform movements.

  • Are a common finding in Huntington disease, Sydenham chorea, and multiple system atrophy
  • Are involuntary, rapid, regular, jerky movements
  • May affect the face, arms, legs, or trunk, or a combination these body parts
  • Are violent flinging movements

Ballismus

Ballismus, also known as ballism, is a violent flinging movement of a limb or limbs. The examination should include delineation of the involved body part, whether the movements occur on a continuous or intermittent basis, and whether the movements are restricted to one side of the body (hemiballism) or occur on both sides. These movements are not typically isolated findings; instead, patients most likely have a variety of movements, including ballismus, chorea, athetosis, and dystonia. Note should be made of any other associated movements.

Myoclonus

The movements of myoclonus consist of sudden, brief, shock-like movements. Positive myoclonus results in contraction of a muscle or multiple muscles. Asterixis, or negative myoclonus, occurs with brief momentary loss of agonist muscle tone and subsequent contraction of antagonist muscles. These nonsuppressible movements often have a characteristic saw-tooth pattern. During the examination, note should be made of the affected body part and the amplitude and persistence of the movements. Spontaneity of movements and provocative factors should be elicited during the exam. Movements may be provoked by having patients sit with their arms outstretched or by flicking the patients' distal finger joints and observing any responsive movement. The examiner may also clap her or his hands and note the patients' response. The examiner should note whether the movements are induced via action or whether a flapping motion, indicative of asterixis, is present. In addition, a movement score can be calculated by measuring the number of jerks over a set period of time, e.g., 60 to 120 seconds.

Inspection and Palpation

Most patients with movement disorders do not experience muscle wasting or hypertrophy. The exceptions to this are patients with dystonia, who may develop hypertrophy related to their disease, and disuse atrophy, which may occur in weakened muscles associated with spasticity. Fasciculations, which are involuntary contractions of the muscle fibers innervated by a motor unit, can be visualized as muscle twitches or dimpling under the skin. These fine quivering movements occur more commonly in patients with lower motor neuron disease and not those with movement disorders. Muscle tenderness (myositis) is not typically a finding when assessing the patient with a movement disorder.

Assessing Tone

To properly assess tone (i.e., the baseline amount of muscle resistance to passive movement about a joint), the clinician must move each of the patient's limbs through its full range of motion at two or more joints. Abnormalities of tone that may be encountered include hypotonia, or too little tone, and hypertonicity, an elevated amount of tone. In its extreme state, hypotonicity is referred to as flaccidity.

When hypertonicity is encountered, the next step in the assessment is to determine whether the increased tone is spasticity (which is defined as a velocity-dependent increase in stretch reflexes that results from an upper motor neuron lesion) or rigidity (which results from a lesion or process occurring in the basal ganglia). The difference between the two is in their relationship to directionality and velocity. With rigidity, the examiner feels the increased resistance during flexion and extension. With spasticity, the resistance is more unidirectional -- i.e., only with flexion or extension, but typically not both. With rigidity, the examiner appreciates the difference in increased resistance at all speeds of movement; with spasticity, the examiner detects the resistance at higher velocities -- i.e., the faster the joint is moved, the more resistance that the examiner feels. The point at which the examiner encounters resistance in spasticity is known as the spastic catch. Conversely, when the examiner is encountering resistance while moving a spastic limb through its range of motion, in some patients she or he will reach a point at which the resistance "gives way" -- this is called the clasped knife phenomenon.

Although rigidity is a common finding on examination, patients with Parkinson's disease do not typically report having rigidity per se; instead they may express that they are having stiffness in their shoulders or other muscles or arthritis-like symptoms. Cogwheel rigidity is a particular type of rigidity that is frequently found in patients with Parkinson's disease. When the affected arm is moved through its range of motion at the elbow, the examiner will encounter a ratcheting type sensation, particularly when palpating the biceps tendon. To elicit cogwheel rigidity, it may be necessary for the examiner to ask the patient to mirror the movements that the examiner is performing, i.e., to move his or her arm in the same manner in which the examiner is passively moving the opposite arm.

Assessing Function

When assessing function, it may be necessary to ask the patients to perform the activity -- such as finger, hand, or foot tapping or alternating pronation and supination of the hand -- for some period of time. Characteristic of parkinsonian syndromes is a difficulty with initiating movement. Once initiated, the movements of patients with Parkinson's disease are fairly rhythmic, however, as opposed to those of patients with cerebellar disorder, which have an irregular rhythm. The movements of Parkinson's disease tend to be relatively slow and of a decreased amplitude. Another distinguishing feature, and the purpose of observing the patient for some time, is that patients with Parkinson's disease often have a slowing of movements with repeated performance of the task, whereas patients with cerebellar disorders can typically sustain the speed of movements ad infinitum. Poor accuracy in the movements is characteristic of cerebellar disorders. Patients with Parkinson's disease or other parkinsonian disorders may be unable to perform rapidly alternating pronation and supination as the result of akinesia or rigidity.

Assessing Strength

To detect asymmetry in strength, each muscle group should be tested along with its contralateral counterpart. A 6-point scale, such as the one included below, can be used to rate muscle strength. With the exception of patients who have spasticity, strength should be normal in most if not all movement disorders; in addition, patients with chorea may have what is known as a milkmaid's grip in which there is a fluctuation in grip strength.

Score Finding
5 Normal strength
4* Some resistance but movement is possible
3 Movement is possible against gravity but not against resistance by examiner
2 Movement possible, but not against gravity
1 Muscle flicker but no movement
0 No muscle contraction

*often subdivided as -4, 4, +4

The examiner should also check for drift, which may be indicative of an upper motor neuron lesion (e.g., trauma, MS, stroke). When patients with an upper motor neuron lesion are asked to extend their arms, suppinate their hands, and hold them parallel to the floor, they may have a subtle turning in and downward drift.

Assessing Posture

Posture is typically assessed by having the patient stand, while the examiner looks for sway or instability. Any movement disorder that is the result of a cerebellar dysfunction will result in ataxia, a swaying unstable posture. Postural instability is a common finding in Parkinson's disease and in other atypical parkinsonian syndromes, such as PSP. The examiner can test for instability by standing behind the patient and asking the patient to maintain her or his balance. The examiner then attempts to briskly pull the patient back while being careful to prevent the patient from falling. Note should be made of the results of this pull test, i.e., the patients ability to recover from being pulled backward. The examiner should also ask the patient to stand with his or her eyes closed, and note should be make of any ataxia.

 

Reflexes

The next step in the examination of the neurologic system is an assessment of reflexes in all four limbs, noting both the strength of the reflex as well as the symmetry. Abnormal reflexes may be manifest as the result of derangements in electrolyte levels or thyroid functioning or in patients who are anxious; reflexes also tend to decrease with advancing age. Deep tendon reflexes are rated as per the table below and are considered normal if they are symmetrical and rated between 1+ and 3+. Asymmetrical reflexes or a substantial difference in reflexes between the upper and lower limbs are indicative of the need for further study.

Score Finding
0 Absent reflex
1+ Trace, or seen only with reinforcement
2+ Normal
3+ Brisk
4+ Nonsustained clonus
5+ Sustained clonus

The presence of clonus, a series of sustained rhythmic jerks following quick stretch of a muscle, usually indicates an upper motor neuron abnormality. Attempts should be made to elicit clonus whenever hyperreflexia is encountered. To test for clonus, the examiner should hold the patient's foot and lower leg in a relaxed position and quickly dorsiflex the ankle. While maintaining the leg in a dorsiflexed position, the examiner will feel the rapid oscillation of the flexion and extension of the foot when clonus is present.

 

Gait abnormalities are a common finding in patients with movement disorders. The first stage in assessing the gait disturbances is to simply observe the patient. The examiner should watch closely as the patient is seated in a chair and then rises to a standing position. Patients with Parkinson's disease or other movement disorders that cause a loss of strength in the lower limbs will often need to use more upper body muscles to rise from a chair, as opposed to relying on their leg strength to stand. Note should be made of the patient's standing posture; approximately 75% of patients with Parkinson's disease will lean forward from the waist, resulting in instability.

The examiner should then observe the patient walking across the room or down the hall, noting the stride length, positioning of the feet, degree of arm swing, presence of abnormal movements, momentum, and ability to turn smoothly. Patients should be asked to walk in a heel-to-toe fashion along a line (tandem gait), to walk on their toes, and to walk on their heels.

Gait difficulties are a common finding in Parkinson's disease, but are typically not one of the early manifestations of the disease. These difficulties with ambulation include postural instability, as well as a freezing gait, diminished or absent arm swing, festination, and hesitancy with initiation of movement. When patients with Parkinson's disease have a freezing episode, they literally become rooted in place, feeling as if their feet are stuck to the floor. Freezing often occurs when patients attempt to walk through a doorway or turn around. The forward-flexed posture of Parkinson's disease combined with a festinating (accelerating) gait leads to the typical propulsive gait in which patients take small, rapidly accelerating, shuffling steps with their weight on the ball of the foot. Leaning forward may be a manifestation of the patient's difficulty with initiating movements, such that the patient leans further and further forward in an attempt to begin walking. (See video example of gait in Parkinson's disease.)

The parkinsonian gait should be distinguished from the apraxic gait, which results from bilateral dysfunction in the frontal lobes. Patients with an apraxic gait also have a stooped posture and short shuffling steps. Their difficulties in initiating and maintaining walking are the result of deficits in executive functioning. When asked to walk, patients with an apraxic gait appear to forget how to initiate the movement and often stop walking for no apparent reason. The examiner should also discriminate between the parkinsonian gait and that of patients with normal pressure hydrocephalus, which is a broad-based gait that also may include the parkinsonian-like features of hesitancy of initiation of movement and freezing but more closely resembles an apraxic gait.

Patients with Huntington disease and other forms of chorea typically have intermittent, involuntary, irregular jerky movements and slow writhing movements of both upper and lower extremities that interrupt the normal flow of walking; this is known as a choreoathetotic gait. Additional movements tend to be lurching in quality as the result of unpredictable flexion and extensions at the hip.

Patients with spasticity of the lower limbs may exhibit one of a variety of abnormal gaits. A steppage gait, also known as a foot-drop gait, is one in which the toes hang down and drag on the floor while the patient is walking. Spasticity may also cause a scissoring gait, in which the legs are flexed slightly at the hips and knees, such that the patient appears to be crouching, with the knees and thighs hitting or crossing in a scissors-like movement. A typical hemiparetic gait involves a fisting of the hand with the arm held in a flexed position and a circumduction of the leg.

Patients with cerebellar ataxia walk with a broad-based gait with irregular stride lengths and speeds. Those with a sensory ataxic gait have a similar gait but also have a positive Romberg sign when tested with their eyes closed.

 

Sensory System

Assessment of the sensory system, i.e., light touch, vibration, and joint-position sense (proprioception) are typically normal in patients with movement disorders. One exception, however, is restless legs syndrome, in which abnormalities have been identified in central somatosensory processing, including static mechanical hyperalgesia.

 

CLOZAPINA + ARIPRIPRAZOL in SCH.

Bachmann CJ et al. - In adolescents with schizophrenia, aripiprazole augmentation of clozapine treatment might be an effective therapeutic strategy. Prospective studies for this age group are required to obtain more specific clinical data on clinical effectiveness.

Methods
  • We included 15 patients with schizophrenia from a child and adolescent psychiatric department (8 male; mean age 19.3 [SD±1.2, range 17.2-21.2] years).
  • Patients had been under clozapine treatment, followed by aripiprazole augmentation.
  • Retrospectively, patients' medical records were reviewed, using a rating scale in analogy to the Clinical Global Impressions (CGI) scale.
Results
  • Mean observation time was 11.1 [SD±9.7] months.
  • Mean CGI-Severity scores improved significantly (p=0.003, d=0.76) from 5.3 (baseline) to 4.5 (endpoint; last observation carried forward (LOCF)).
  • CGI-Improvement scores decreased from 3.7 (after 1 month) to 3.3 (endpoint; LOCF) (p=0.212, d=0.45).

OLANZAPINA > VALPROAT in MANIE

  • Novick D et al. - The EMBLEM results support those of the RCT, which suggest that olanzapine monotherapy seems to be more effective than valproate monotherapy in the treatment of acute mania.
Methods
  • EMBLEM (European Mania in Bipolar Evaluation of Medication) was a 2-year, prospective, observational study of health outcomes associated with the treatment of mania.
  • Severity of mania and depression were assessed at baseline and 6 weeks using the YMRS and the 5-item version of the HAMD, respectively.
Results
  • 621 patients were analysed (n=107 valproate, n=514 olanzapine).
  • Both groups improved from baseline to 6 weeks in mean YMRS and HAMD-5 total scores, with greater mean improvements in the olanzapine compared with the valproate group.
  • Olanzapine was associated with more weight gain and less gastrointestinal difficulties than valproate.

TRATAMENT PARKINSON

http://cme.medscape.com/viewarticle/704043?src=cmemp

APA 2009: Alcoholism Is Not What It Used to Be

 

APA 2009: Alcoholism Is Not What It Used to Be, Expert Says

(MedScape video)

 

http://www.medscape.com/viewarticle/703483?src=emailthis

 

Psychiatry Research Round-up

Psychiatry Research Round-up: The Best of APA 2009

http://www.medscape.com/viewarticle/704237?src=top10

 

EDITORIAL OPORTUNISM IN PSIHIATRIE

Enescu a spus: serviti muzica, nu va serviti de ea! Aceeasi recomandare e valabila si in psihiatrie. Nu rareori am auzit tineri psihiatri spunind ca au venit in meserie din vocatie, dar viata arata ca ei nu se ocupa de bolnavul psihic ci doar sa cistige sa-si ia masina, excursii, casa secundara etc. Scopul scuza mijloacele si stunci nu mai conteaza teoria, idealul, binele bolnavului, scopurile cursei lungi ci viata ca plezirism. Dupa noi potopul... Cei care urmeaza pe Enescu, n-au divertisment de vara. Ei gindesc, au cite o idee, formuleaza o ipoteza, se gindesc la o lucrare pentru un congres de toamna, o carte. Profesia te multumeste daca urmaresti o reechilibrare durabila a bolnavului, asta este muzica clasica a resocializarii pe care o veti auzi dupa infringerea, fie si partiala a oprtunismului care a pus mina pe psihiatrie cu firme cu tot.

                                   Prof.Romila

MDS 2009: Memantine May Benefit Parkinson's Disease Dementia and Dementia With Lewy Bodies

From Medscape Medical News

MDS 2009: Memantine May Benefit Parkinson's Disease Dementia and Dementia With Lewy Bodies

Susan Jeffrey

 
 

June 18, 2009 — Results of a randomized phase 2 trial suggest that patients with dementia associated with Parkinson's disease (PDD) or dementia with Lewy bodies (DLB) may benefit from treatment with memantine (Ebixa/Abixa, Lundbeck), an agent already approved for use in moderate to severe Alzheimer's disease.

"This is the first positive randomized, placebo-controlled trial of memantine in patients with Parkinson's dementia and dementia with Lewy bodies," lead author Dag Aarsland, MD, from the Norwegian Center for Movement Disorders at Stavanger University Hospital, told Medscape Neurology; it showed a positive response with treatment on the primary end point of improvement on the Clinical Global Impression of Change (CGIC) in these patients.

"We are excited about this, and although it's a small study, the findings are very encouraging and should lead to follow-up studies with a larger number of patients to confirm them," he added.

Dr. Aarsland presented the results at the Movement Disorders Society's 13th International Congress of Parkinson's Disease and Movement Disorders. The study was published online June 10 in the Lancet Neurology to coincide with the presentation and will appear in the July issue.

This clinician-initiated study was supported by the Western Norway Regional Health Authority and Lundbeck. Memantine is also marketed as Namenda (Forest Pharmaceuticals), Axura/Akatinol (Merz Pharmaceutical), andMemox (Unipharm).

Common Dementias

DLB and PDD are common forms of dementia that have a major impact on quality of life, the authors write. "Only rivastigmine [Exelon, Novartis] is licensed for PDD, and there are no treatments for DLB," they note.

These 2 dementias are separate clinical entities, Dr. Aarsland noted, "but they are very similar in terms of what we know about clinical symptoms and pathological changes. Both dementias are dominated by Lewy bodies in the cortex of the brain, and also there are some Alzheimer's changes, although less pronounced than you would find in Alzheimer's disease."

Memantine, an N-methyl-D-aspartate (NMDA)–receptor antagonist, is already approved for use in moderate to severe AD, but the precise mechanism of improvement is not clear, he noted. "We know that the major mode of mechanism is that it normalizes glutamatergic neurotransmission," he said. "It might also influence in a positive way the dopaminergic transmission, which might be particularly relevant for this patient group."

It's possible that memantine may also have neuroprotective effects, "but that is more speculative," Dr. Aarsland added.

The current study was a parallel-group, 24-week randomized and placebo-controlled pilot study that included 75 patients with PDD and DLB from 4 centers in Sweden, Norway, and the United Kingdom. They were randomized to receive either 20 mg per day of memantine or placebo. The primary outcome was change on the CGIC scale; scores on this scale range from 1 to 7 points, with a lower score indicating a better outcome.

Of the 75 patients, 56 completed the study. All withdrawals were due to adverse events, but the proportion was similar between the treatment groups and in fact was slightly higher in the placebo group, Dr. Aarsland noted.

There was no particular pattern for dropouts, he added, with reasons including worsening of disease, urinary tract infection, and others. "The mean age of this group was 77 years old, so these are old, frail people with parkinsonism and dementia," he said. Analysis was by intention-to-treat, using the last observation carried forward.

At week 24, a significant difference between groups was found on the CGIC, with a mean difference of 0.7 points (95% CI, 0.04 – 1.39; P = .03). With the exception of improved speed on attentional tasks in the memantine group, specifically a quick test-of-cognition form, with a difference of 12.4 (P = .004), there were no significant differences between groups in secondary outcome measures.

Large-scale phase 3 studies are now needed to determine the real benefit of this treatment in these patients, Dr. Aarsland added. Their group is not involved in this ongoing work at this time, "so it's up to the company to provide more confirmative data from a larger trial," he said.

A "Welcome Addition"

In a Reflection and Reaction commentary accompanying the paper in Lancet Neurology, Murat Emre, MD, from the Istanbul Faculty of Medicine, in Turkey, calls this trial "a welcome addition in the treatment of patients with Lewy body–related disorders, in whom the options are scarce."

Dr. Emre points, though, to some limitations of the study, including a high attrition rate, a relatively low sample size for each of the 2 conditions studied, and background therapy with cholinesterase inhibitors, with which an interaction cannot be ruled out. In addition, there was an imbalance in this and other background therapies, including antipsychotics and antiparkinsonian drugs, between the groups.

Still, Dr. Emre writes, the effect size was "reasonably robust," mostly due to improvements in the patients with PDD.

"Although not conclusive, these results are encouraging, but they await confirmation before memantine can be added to the list of treatments for these patients," Dr. Emre concludes. "A larger, randomized placebo-controlled, multicenter trial including 199 patients with either DLB or PDD has just been completed, and the results are being analyzed. Should these results of Aarsland and colleagues be confirmed, the choices of treatment for physicians managing such patients might be expanded."

"Small but Significant" Change

Asked for comment on these findings, Steven J. Frucht, MD, from the movement-disorders division of the Neurological Institute of New York at Columbia University, said he would classify the change achieved by treatment in this trial as "small but significant."

"Whether or not this amounts to a noticeable difference in daily functioning remains to be seen," Dr. Frucht toldMedscape Neurology. "Also, whether or not tolerability will be as good in a general population outside of a trial is a concern," he added, "but still, promising."

This investigator-initiated study was supported by Lundbeck and the Western Norway Regional Health Authority. Dr. Aarsland reports he has received honoraria and research support from Lundbeck, Novartis, GE Healthcare, and Merck-Serono. Disclosures for coauthors appear in the paper. Dr. Emre reports he has been on advisory committees for and received consultancy fees, honoraria, or study grants from Boehringer Ingelheim, Schering-Plough, Esai, Pfizer, Lundbeck, Merck-Serono, Noscira, and Novartis.

13th International Congress of Parkinson's Disease and Movement Disorders, Paris, France: Abstract LB-02. Presented June 10, 2009.

MDS 2009: Personality Traits Do Not Influence Parkinson's Disease Risk

From Medscape Medical News

MDS 2009: Personality Traits Do Not Influence Parkinson's Disease Risk

Pauline Anderson

June 23, 2009  A new study has shown no link between either high or low novelty-seeking personality traits exhibited in younger years and the risk of developing parkinsonism or Parkinson's disease (PD) later in life.

For decades, there has been speculation that there may be a distinctive "parkinsonian personality" associated with an increased risk for the disease. According to this theory, a person at risk for eventually developing Parkinson's disease is morally rigid, introverted, punctual, cautious, and conventional. However, results of the new study show no association between PD development and the presence of either with high or low novelty-seeking traits.

"We provided the first evidence that it's not possible to recognize people at risk of Parkinson's disease many years before they develop the disease itself on the basis of their personality traits," said Gennarina Arabia, MD, from the Mayo Clinic in Rochester, Minnesota and the Institute of Neurology at the Università degli studi Magna Græcia di Catanzaro, in Italy, who led the investigation.

Their findings were presented during the Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders, in Paris, France.

Historical Cohort

This study is part of the growing body of research that aims to determine whether personality traits precede PD symptom onset and increase risk for this condition.

Dr. Arabia and her colleagues established a historical cohort of 7216 subjects who completed the Minnesota Multiphasic Personality Inventory (MMPI) at the Mayo Clinic from 1962 through 1965. Of these, 6822 (94.5%) were followed for over 40 years either through phone interviews with the subject or a close relative or by means of archived records or death certificates. During follow-up, 227 patients developed parkinsonism, of whom 156 were diagnosed with PD.

The researchers used 5 MMPI scales (sensation-seeking, hypomania, positive emotionality, constraint, and social-introversion scales) to examine the role of novelty-seeking personality traits in the development of PD. Features of the so-called "at-risk" personality, including moral rigidity, etc, are included in these scales, said Dr. Arabia.

The investigators found no association between sensation seeking and an increased risk for PD. They also found no link between PD and hypomania, positive emotionality, constraint, or social-introversion traits.

"In our study, we investigated the risk of developing PD correlated with all the possible scores of the scales for novelty seeking — from low to high scores," said Dr. Arabia in an email interview. "There was no association with either low or high degree of novelty-seeking personality traits."

While this research has no immediate clinical implications and probably will not result in any new recommendations for physicians, the findings do open new areas of exploration related to the issue of personality and PD, said Dr. Arabia. 

Impulse Control

For example, she noted, there is growing interest in studying impulse-control disorders displayed by some PD patients who take dopaminergic drugs. These disorders involve pathological gambling, hypersexuality, compulsive eating, and compulsive buying — behaviors that could have an important social impact, said Dr. Arabia.

"It would be of great interest to investigate the link between the premorbid novelty-seeking personality and the later development of these dopaminergic drug-related compulsive behaviors in PD patients," she told Medscape Neurology.

Dr. Arabia and her colleagues plan to take advantage of their cohort of over 7000 subjects who completed the MMPI and have been followed for over 4 decades to explore the association of some of these other personality traits and PD. 

No Definitive Answers

Asked for a comment, Rajesh Pahwa, MD, Laverne and Joyce Rider professor of neurology and director of the Parkinson Disease and Movement Disorder Center at the University of Kansas Medical Center, in Kansas City, said that while the topic is "interesting," the current study does not definitively answer the question of what role personality traits play in PD.

"More prospective studies are required with more vigorous criteria for both the diagnosis of PD and assessing the premorbid personality traits," he said.

Dr. Arabia reports no conflict of interest.

Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders, Paris France: Abstract 160. Presented June 8, 2009.

FILOZOFIE SI PSIHOPATOLOGIE

Philosophy of Psychopharmacology

by Dan J. Stein. New York, Cambridge University Press, 2008, 224 pp., $60.00.

STEVEN L. DUBOVSKY, M.D.
Buffalo, N.Y.

Developing effective psychiatric interventions depends on identifying specific targets for these interventions. Traditionally, such targets have been diagnoses, but most of the treatments we have work for more than one disorder. The more data we have on the features of diverse disorders on which a particular treatment acts, the more precise our treatments become.

This book, written by the chair of the Department of Psychiatry at the University of Cape Town, who is also—or perhaps primarily—a philosopher, expands the question of who should get what treatment by addressing several fundamental questions. Among the issues raised are: To what degree are psychiatric disorders valid independent constructs versus culturally defined misalignments between the individual and society? What happens to the identity of the person whose point of view is changed by medications or psychotherapy? What are the borders at which psychiatric treatment becomes cosmetic rather than clinical? Although it is advertised as a book on psychopharmacology, there are coordinated discussions of the nature and meaning of psychotherapy as well as nonpsychiatric treatments such as meditation.

The book contains extensive scholarly syntheses of the psychiatric and philosophical literature. Mercifully for those of us who are less informed about the philosophical concepts that are discussed, each new chapter summarizes what was said in the last one. The only issue that is missing is whether current categorical concepts of diagnosis will ultimately prove useful in guiding treatment or whether discrete dimensions such as endophenotypes or specific traits will turn out to be more useful in choosing a particular treatment.

This book will be especially appealing to people who liked college philosophy and want to have another go at it in a more condensed format that is a little more relevant to their work.

For many clinicians, delving into the ultimate meaning of making diagnoses, prescribing treatment, and changing people may feel a bit like driving a car on a busy freeway while contemplating why the road has eight lanes, what the laws of physics are that make the car run, whether an alternative-fuel vehicle would work better, what forces led to our insistence on driving everywhere ourselves and using up so much oil, and so on. These are important questions that may have an impact on where we will drive next, but if we reason all this out while negotiating traffic, we may feel distracted and might even miss our exit.

The gap between everyday practice and the ultimate meaning of what we do as clinicians was brought home to me when a very capable neurologist friend of mine told me about a patient he had just referred. "Perhaps you can explain the question she asked me," he said. "She wanted to know what your philosophy was. ‘Is he a psychopharmacologist, a behaviorist, a Freudian, a Jungian, or a cognitive therapist? What is his orientation toward mental illness?’"

BIPOLARA si DEPRESIA MAJORA

ICBD 2009: fMRI Differentiates Bipolar from Major Depression

Janis Kel

July 1, 2009 — A new study using neuroimaging has identified neural system biomarkers that differentiate depression in early bipolar disorder from major depression and might be able to identify "at-risk" children early enough to permit psychotherapy that could alter the course of the disease.

Mary L. Phillips, MD, professor of psychiatry and director of functional neuroimaging in emotional disorders at the University of Pittsburgh School of Medicine, in Pennsylvania, discussed the imaging research at the 8th International Conference on Bipolar Disorder.

"Bipolar disorder is difficult to diagnose if the patient presents with depression and no history of being manic or 'high.' That matters, because it leads to inappropriate treatment with antidepressants and delay in treatment with mood stabilizers, which in turn can make the risk of switching to the manic phase greater," Dr. Phillips told Medscape Psychiatry. "We have shown that neuroimaging with functional magnetic resonance imaging [fMRI] can be used to differentiate major depression from depression in bipolar disorder."

The biomarkers Dr. Phillips and colleagues identified pertain to areas in the amygdala and orbitomeatal prefrontal cortex (OMPFC) involved in the emotional dysregulation associated with bipolar disorder. When they compared scans of subjects who were asked to label the emotional intensity of happy and sad faces, the researchers found that those with bipolar disorder had brain changes that reduced left-sided regulation of the amygdala by OMPFC. This might indicate a predisposition to elevated mood and mania, they speculate.

By contrast, subjects with major depressive disorder had overregulation of the amygdala in response to positive emotional stimuli, which might cause a reduced ability to respond to positive emotions. These subjects also had an exaggerated response to negative emotional stimuli.

Dr. Phillips noted that bipolar depression is the most frequent presentation of bipolar disorder and that 35% of bipolar individuals do not receive a correct diagnosis for more than 10 years after symptoms begin, so a reliable noninvasive diagnostic test would have major clinical implications. Only 20% of bipolar-disorder cases are correctly diagnosed within the first year of the patient seeking treatment.

Children of patients who are diagnosed with bipolar disorder are at 10-fold higher risk for the disorder than the general population. Dr. Phillips said that her research team is now "working backward in time" by using fMRI to examine the offspring of bipolar-disorder patients.

"We have data showing that certain fMRI abnormalities in otherwise-healthy offspring are similar to what we see in adults with bipolar disorder," Dr. Phillips said. "We are now following these children to see which ones go on to develop bipolar disorder. If these neuroimaging markers do identify that subgroup, it might enable us to intervene early with psychotherapy and try to intervene in the abnormal developmental pathway, perhaps preventing or reducing the severity of disease."

Dr. Phillips collaborated on these neuroimaging studies with Drs. David Axelson and Boris Birmaher.

Identifying Those at Risk

Jonathan Savitz, MD, told Medscape Psychiatry that Dr. Phillips's discoveries might be very useful for researchers as well as clinicians.

"The ability to identify high-risk individuals with neuroimaging would be a wonderful advance, because it would tell us something about the underlying neuropathology of the disorder and help inform genetic studies," said Dr. Savitz, who is in the section on neuroimaging in the Mood and Anxiety Disorders Program at the National Institute of Mental Health, in Bethesda, Maryland

Challenges in Depression Treatment - MedScape video

Challenges in Depression Treatment: Finding the Right Augmentation Strategy

 ( MedScape video )

 

http://cme.medscape.com/viewarticle/704390?src=emailthis

 

*Trebuie LogIn sau inregistrare nume utilizator pe adresa : www.medscape.com  pentru vizualizare.

 

 

BJP -- FUTURE Table of Contents

Fwd: The British Journal of Psychiatry Future Table of Contents for 1 August 2009; Vol. 195, No. 2



NEW from the ROYAL COLLEGE of PSYCHIATRISTS  CPD Online  The NEW online learning resource for mental health professionals:

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *
improve your knowledge and keep up to date with research and best
practice guidelines in psychiatry.
* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

BJP -- Future Table of Contents Alert

A new future TOC for The British Journal of Psychiatry is available online for the issue:
August 2009; Vol. 195, No. 2

This Future Table of Contents is available online at:http://bjp.rcpsych.org/future/195.2.shtml 







Editorials

Dissecting the phenotype in genome-wide association studies of psychiatric illness
Cross-Disorder Phenotpye Group of the Psychiatric GWAS Consortium
The British Journal of Psychiatry 2009 195 (2)

Do prenatal risk factors cause psychiatric disorder? Be wary of causal claims
A. Thapar and M. Rutter
The British Journal of Psychiatry 2009 195 (2)


Special article
Why do antidepressants take so long to work? A cognitive neuropsychological model of antidepressant drug action
C. J. Harmer, G. M. Goodwin and P. J. Cowen
The British Journal of Psychiatry 2009 195 (2)


Review article
Residential alternatives to acute psychiatric hospital admission: systematic review
B. Lloyd-Evans, M. Slade, D. Jagielska and S. Johnson
The British Journal of Psychiatry 2009 195 (2)


Papers
Levels of anxiety and depression as predictors of mortality: the HUNT study
A. Mykletun, O. Bjerkeset, S. Overland, M. Prince, M. Dewey and R. Stewart
The British Journal of Psychiatry 2009 195 (2)

Differencess in mortality and suicidal behaviour between treated and never-treated people with schizophrenia in rural China
M.-S. Ran, C. L.-W. Chan, E. Y.-H. Chen, W.-J. Mao, S.-H. Hu, C.-P. Tang, F.-R. Lin and Y. Conwell
The British Journal of Psychiatry 2009 195 (2)

Early-life origins of schizotypal traits in adulthood
J. Lahti, K. Raikkonen, U. Sovio, J. Miettunen, A.-L. Hartikainen, A. Pouta, A. Taanila, M. Joukamaa, M.-R. Jarvelin and J. Veijola
The British Journal of Psychiatry 2009 195 (2)

Childhood neuropsychological deficits associated with adult obsessive-compulsive disorder
J. R. Grisham, T. M. Anderson, R. Poulton, T. E. Moffitt and G. Andrews
The British Journal of Psychiatry 2009 195 (2)

Impact of childhood exposure to a natural disaster on adult mental health: 20-year longitudinal follow-up study
A. C. McFarlane and M. Van Hooff
The British Journal of Psychiatry 2009 195 (2)

Association between common mental disorder and obesity over the adult life course
K. Kivimaki, G. D. Batty, A. Singh-Manoux, H. Nabi, S. Sabia, A. G. Tabak, T. N. Akbaraly, J. Vahtera, M. G. Marmot and M. Jokela
The British Journal of Psychiatry 2009 195 (2)

Urbanicity of place of birth and symptoms of psychosis, depression and anxiety in Uganda
P. Lundberg, E. Cantor-Graae G. Rukundo, S. Ashaba and P.-O. Ostergren
The British Journal of Psychiatry 2009 195 (2)

Morphometric analysis of neuronal and glial cell pathology in the dorsolateral prefrontal cortex in late-life depression
A. Khundakar, C. Morris, A. Oakley, W. McMeekin and A. J. Thomas
The British Journal of Psychiatry 2009 195 (2)

Measuring the benefits of treatment for psychosis: validity and responsiveness of the EQ-5D
G. R. Barton, J. Hodgekins, M. Mugford, P. B. Jones, T. Croudace and D. Fowler
The British Journal of Psychiatry 2009 195 (2)

AJP Anunt

Stimati psihologi, 


In perioada 18 iunie – 1august  va puteti abona la publicatia de specialitateAmerican Journal of Psychotherapy pentru anul 2009.

Cele patru numere ale anului 2009 pot fi achizitionate prin abonament, pretul acestuia fiind de 100 lei, precum si din comertul de carte (pret pe exemplar 30 lei). 
Plata poate fi facuta prin mandat postal sau ordin de plata in contul RO54BRDE445SV12328744450, deschis la BRD Sucursala VICTORIA Bucuresti.
Dovada platii se poate face la adresa de e-mail:cristina.popescu@edituratrei.ro  ori telefonic la : 021 300 60 90.
Pentru mai multe informatii va rog sa intrati pe urmatorul link:http://www.edituratrei.ro/abonament.php

American Journal of Psychotherapy ofera informatii, comentarii si dezbateri despre principalele orientari din psihoterapia contemporana (comportamentala, psihodinamica, spirituala si experentiala). Prezentarile de cazuri abunda, tehnica, dar si teoriile psihologice intemeietoare bucurandu-se de o deosebita atentie. Prestigiul revistei este ilustrat nu numai de indelungata sa traditie, dar si de personalitatile care ii alcatuiesc board-ul, printre care se numara Aaron T. Beck, Arnold Lazarus, Glen O. Gabbard, Irwin Yalom, Otto Kernberg. 

AJP in Advance Articles

American Journal of Psychiatry AJP in Advance Alert

New American Journal of Psychiatry AJP in Advance articles have been made available
(for the period 10 Jun 2009 to 15 Jun 2009):
 

 

Articles

Sudden Death and Use of Stimulant Medications in Youths
Madelyn S. Gould, B. Timothy Walsh, Jimmie Lou Munfakh, Marjorie Kleinman, Naihua Duan, Mark Olfson, Laurence Greenhill, and Thomas Cooper
Am J Psychiatry published 15 June 2009, 10.1176/appi.ajp.2009.09040472
http://ajp.psychiatryonline.org/cgi/content/abstract/appi.ajp.2009.09040472v1
 

 

Reducing Suicidal Ideation and Depression in Older Primary Care Patients: 24-Month Outcomes of the PROSPECT Study
George S. Alexopoulos, Charles F. Reynolds, III, Martha L. Bruce, Ira R. Katz, Patrick J. Raue, Benoit H. Mulsant, David W. Oslin, Thomas Ten Have, and The PROSPECT Group
Am J Psychiatry published 15 June 2009, 10.1176/appi.ajp.2009.08121779
http://ajp.psychiatryonline.org/cgi/content/abstract/appi.ajp.2009.08121779v1


Editorials

Stimulant Treatment of ADHD and Risk of Sudden Death in Children
Benedetto Vitiello and Kenneth Towbin
Am J Psychiatry published 15 June 2009, 10.1176/appi.ajp.2009.09050619
http://ajp.psychiatryonline.org/cgi/reprint/appi.ajp.2009.09050619v1

HOME (*Revenire-Pagina la Zi)

MENU

EDITORIAL