What does psychomotor mean? What are some examples?

Question

I will be working with small children for the rest of the summer and overheard some of my superiors talking about psychomotor skills. I seemed to be the only one who didnt know what that was. Can any one clarify for me?

Answer 1

Psychomotor skills are those skills that you have done so often that you don't think about how to do them while you are doing them. As well as tying shoelaces, riding a bike is another example. At first, you really have to concentrate on the steps, later your brain takes over.

Answer 2

Basically it's about brain-body coordination.  I was trying to think how to explain it, and found a good explanation here:

Macmillan English Dictionary: Psychomotor Skills

The learning of complex sequences of actions that require perceptual information (input from the eyes, for example) and control of the muscles.

Example:

Learning to tie shoelaces.

The child needs to process the following information:

    * from the eyes (where are the shoelaces?)

    * from the fingers (what shape are the shoelaces under the fingers? How tight is the knot?, etc)

They then need to combine this information with controlling the muscles of the fingers and hands to move the shoelaces in the correct way.

Answer 3

Psychomotor includes physical and motor fitness. The numerous activities included in psychomotor must enhance both the preschooler's physical fitness and motor fitness. Included under the two terms are such elements as strength, flexibility, endurance, balance, speed, and coordination.

Examples are how to ride a bike, using balance beam, how to tie shoe laces, folding activities, jump over rope, and the like..

hope this can somehow help you undersand this concept.

Answer 4

from what i have read,psychomotor epilepsy is another name for temporal lobe epilepsy............... Background: Temporal lobe epilepsy (TLE) was defined in 1985 by the International League Against Epilepsy (ILAE) as a condition characterized by recurrent unprovoked seizures originating from the medial or lateral temporal lobe. The seizures associated with TLE consist of simple partial seizures without loss of awareness (with or without aura) and complex partial seizures (ie, with loss of awareness). The individual loses awareness during a complex partial seizure because the seizure spreads to involve both temporal lobes, which causes impairment of memory.

TLE was first recognized in 1881 by John Hughlings Jackson, who described "uncinate fits" and the “dreamy state." In the 1940s, Gibbs et al introduced the term "psychomotor epilepsy." The international classification of epileptic seizures (1981) replaced the term psychomotor seizures with complex partial seizures. The ILAE classification of the epilepsies uses the term temporal lobe epilepsy and divides the etiologies into cryptogenic (presumed unidentified etiology), idiopathic (genetic), and symptomatic (cause known, eg, tumor).

Pathophysiology: Hippocampal sclerosis is the most common pathologic finding in TLE. Hippocampal sclerosis involves hippocampal cell loss in the CA1 and CA3 regions and the dentate hilus. The CA2 region is relatively spared.

History:

Aura

Auras occur in approximately 80% of temporal lobe seizures. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Auras may be classified by symptom type; the types comprise somatosensory, special sensory, autonomic, or psychic symptoms.

Somatosensory and special sensory phenomena

Olfactory and gustatory illusions and hallucinations may occur. Acharya et al found that olfactory auras are associated more commonly with temporal lobe tumors than with other causes of TLE.

Auditory hallucinations consist of a buzzing sound, a voice or voices, or muffling of ambient sounds. This type of aura is more common with neocortical TLE than with other types of TLE.

Patients may report distortions of shape, size, and distance of objects.

These visual illusions are unlike the visual hallucinations associated with occipital lobe seizure in that no formed elementary visual image is noted, such as the visual image of a face that may be seen with seizures arising from the fusiform or the inferior temporal gyrus.

Things may appear shrunken (micropsia) or larger (macropsia) than usual.

Tilting of structures has been reported. Vertigo has been described with seizures in the posterior superior temporal gyrus.

Psychic phenomena

Patients may have a feeling of déjà vu or jamais vu, a sense of familiarity or unfamiliarity, respectively.

Patients may experience depersonalization (ie, feeling of detachment from oneself) or derealization (ie, surroundings appear unreal).

Fear or anxiety usually is associated with seizures arising from the amygdala.

Patients may describe a sense of dissociation or autoscopy, in which they report seeing their own body from outside.

Autonomic phenomena are characterized by changes in heart rate, piloerection, and sweating. Patients may experience an epigastric "rising" sensation or nausea.

Physical:

Following the aura, a temporal lobe complex partial seizure begins with a wide-eyed, motionless stare, dilated pupils, and behavioral arrest. Oral alimentary automatisms such as lip smacking, chewing, and swallowing may be noted. Manual automatisms or unilateral dystonic posturing of a limb also may be observed.

Patients may continue their ongoing motor activity or react to their surroundings in a semipurposeful manner (ie, reactive automatisms). They can have repetitive stereotyped manual automatisms.

A complex partial seizure may evolve to a secondarily generalized tonic-clonic seizure.

Patients usually experience a postictal period of confusion, which distinguishes TLE from absence seizures, which are not associated with postictal confusion. In addition, absence seizures are not associated with complex automatisms. Postictal aphasia suggests onset in the language-dominant temporal lobe.

Most auras and automatisms last a very short period—seconds or 1-2 minutes. The postictal phase may last for a longer period (several minutes). By definition, amnesia occurs during a complex partial seizure because of bilateral hemispheric involvement.

Causes:

Approximately two thirds of patients with TLE treated surgically have hippocampal sclerosis as the pathologic substrate.

The etiologies of TLE include the following:

Past infections, eg, herpes encephalitis or bacterial meningitis

Trauma producing contusion or hemorrhage that results in encephalomalacia or cortical scarring

Hamartomas

Gliomas

Vascular malformations (ie, arteriovenous malformation, cavernous angioma)

Cryptogenic: A cause is presumed but has not been identified.

Idiopathic (genetic): This is rare. Familial TLE was described by Berkovic and colleagues, and partial epilepsy with auditory features was described by Scheffer and colleagues.

Hippocampal sclerosis produces a clinical syndrome called mesial temporal lobe epilepsy (MTLE). MTLE begins in late childhood, then remits, but reappears in adolescence or early adulthood in a refractory form.

Imaging Studies:

MRI is the neuroimaging modality of choice for patients with TLE.

Thin coronal oblique slices of 1.5-2 mm with no gap using spoiled gradient recall images (SPGR) are recommended.

All patients with newly diagnosed TLE should have a high-resolution MRI.

High-resolution MRI shows hippocampal atrophy in 87% of patients with TLE by visual analysis alone. Hippocampal atrophy is bilateral in 10-15% of cases. An increase in the T2-weighted signal intensity in the hippocampus may be seen on fluid-attenuated recovery (FLAIR) MRI; this finding is also consistent with hippocampal sclerosis.

Positron emission tomography with 18-fluorodeoxyglucose (PET-FDG) is a useful tool for interictal seizure localization in surgical candidates when the MRI result is normal.

It usually is performed as an adjunctive measure to delineate the epileptogenic zone.

Interictal deficits include reduced glucose metabolism in the medial and lateral temporal lobe.

Ictal PET recordings are rare.

Single-photon emission computed tomography (SPECT) is also an adjunctive imaging modality useful only for surgical candidates; the accuracy of seizure localization is about 80-90%.

Ictal SPECT done with hexamethylpropyleneamine oxime (HMPAO) shows hyperperfusion in the region of seizure onset. The characteristic pattern is hyperperfusion of the medial and lateral temporal lobe. This requires ictal injection within 30 seconds of seizure onset.

Interictal SPECT testing is less sensitive than FDG-PET and ictal SPECT and is not used routinely for localization of the epileptogenic zone.

Investigational techniques such as MR spectroscopy may become clinically useful in the future in selected surgical candidates with normal MRI.

Other Tests:

Interictal EEG should be performed in all patients with suspected TLE.

Interictal abnormalities, consisting of spike/sharp and slow complexes, usually are located in the anterior temporal region (F7/F8 and T3/T4 electrodes) or basal temporal electrodes (T9/T10 and F9/F10).

One third of patients with TLE have bilaterally independent, temporal interictal epileptiform abnormalities.

Ictal recordings from patients with typical TLE usually exhibit 5-7 Hz, rhythmic, sharp theta activity, maximal in the sphenoidal and the basal temporal electrodes on the side of seizure origin.

In documented temporal lobe seizures, lateralized postictal slowing, when present, is a reliable lateralizing finding.

Video-EEG telemetry is used as part of the presurgical evaluation. It also is used if the diagnosis of TLE is suspected but still in question.

Intracranial EEG with placement of intracranial subdural electrodes is done only if the patient is a surgical candidate and MRI and other non-invasive EEG data are not sufficiently localizing

Medical Care:

About 47-60% of new-onset partial seizures are controlled effectively by the first drug. Studies in 1985 and 1992 by the Department of Veterans Affairs (VA) have shown that the 4 major antiepileptic drugs (AEDs), phenytoin, phenobarbital, carbamazepine, and valproate, are equally effective in controlling partial seizures; however, phenobarbital and valproate have more severe adverse effects.

The newer AEDs, such topiramate, lamotrigine, levetiracetam, oxcarbezapine, and zonisamide have similar if not better efficacy than the older AEDs. In patients with newly diagnosed epilepsy, lamotrigine appears to be significantly better than carbamazepine in terms of tolerability and health-related quality of life issues.

Four other drugs were approved in the year 2000 by the US Food and Drug Administration (FDA) for treatment of partial seizures. These include zonisamide, oxcarbazepine, and levetiracetam.

About 40% of patients continue to have seizures in spite of trials with 3 AEDs. Semah and colleagues showed that seizures are more likely to be refractory to AEDs in patients with hippocampal sclerosis.

Surgical Care:

Vagus nerve stimulation

Vagus nerve stimulation (VNS) was approved by the FDA in 1997 for treatment of intractable partial epilepsy for patients aged 12 years and older. VNS with a high-frequency stimulation rate resulted in a mean reduction in seizure frequency of 25-28%. The exact mechanism by which it exerts its antiepileptic effect is not known. A battery-operated stimulator device is implanted in the left vagus nerve subcutaneously in the neck.

Adverse effects include hoarseness of voice, cough, local pain,