Aphasia, Apraxia and Scotoma

http://www.strokeassociation.org/presenter.jhtml?identifier=3030925

http://en.wikipedia.org/wiki/Scotoma

In a recent posting in the migraine community, someone discussed experiencing Aphasia and Apraxia during migraines. I experience those during most moderate to severe migraines, as well as sensitivity to light and sound (in general I always have a low tolerance to light and sound), along with the normal pain, etc, etc. . I feel like the pain with migraines is the easiest to deal with. But not being able to "find words" in your brain and communicate like normal or pronounce words correctly etc. is devastating. I can often not do a simple addition problem during an attack. The sensitivity to light is a very tough one too because the light is blinding and your vision can literally change. The difference between a migraine and a normal headache is a migraine is absolutely debilitating and really is not so much about the overall pain, but is more like a mini stroke. Also, it can be life threatening when you look at the link between stroke and migraine. From what I have seen, even some cardiologists sometimes have a difficult time differentiating between a TIA and a bad migraine.

I also included the link for Scotoma, also discussed in the posting. That is basically a visual aura, as I discussed in my previous posting. My earliest visual aura that I remember was age 10.

The neurotoxicity and safety of treatment with cefepime in patients with renal failure

Abstract
Background: Cases of cefepime neurotoxicity have been Sporadically reported in patients with renal failure. The neurotoxicity of cefepime might be underestimated and the frequency of its neurotoxic effects may be insufficiently recognized.

Methods: We retrospectively reviewed the files of patients with renal failure who were treated with cefepime and who developed neurological complications.

Results: All 8 patients developed decreased conscience, confusion, agitation, global aphasia, myoclonus, chorea-athetosis, convulsions and coma. The latency, the period between the start of treatment and neurologicaldeterioration, was 4,75 ± 2,55 days (range: 1–10 days). All patients died 17 ± 14,7 days (range: 1–42 days) after becoming symptomatic. Three of them died shortly after neurological deterioration. Five patients developed a neurological "tableau" with global aphasia. Three patients showed clinical improvement after the discontinuation of cefepime. Electroencephalography revealed diffuse slow-wave activity (delta) and triphasic sharp wave activity. These findings confirm the possible neurotoxicity of treatment with cefepime in patients with renal failure. In none of the deceased patients have we been able to directly demonstrate a causal relationship between neurotoxicity and mortality. However, when a patient treated with cefepime develops neurological deterioration or aphasia, one must be aware of cefepime's potential neurotoxicity and treatment should be stopped.

Conclusion: We recommend that, in view of the high and unexplained mortality, the use of cefepime in patients with kidney failure should be carefully considered.

Keywords: cefepime; neurotoxicity; renal failure; kidney disease

Mirror Neurons -- Rock Stars or Backup Singers?

Greg Hickok
Center for Cognitive Neuroscience
University of California, Irvine


Mirror neurons are the rock stars of cognitive neuroscience. Discovered in the mid-1990s by Giacomo Rizzolatti and his colleagues at the University of Parma, these brain cells have been claimed to be the neural basis for a host of complex human behaviors including imitation, action understanding, language, empathy, and mind-reading – not psychic mind-reading, but our capacity to "get inside someone else's head" and imagine how they feel or what they might do. Meanwhile, dysfunction of the mirror neuron system has been linked to developmental disorders, such as autism. With that kind of explanatory range, it's no surprise that mirror neurons have headlined in all forms of news media. But is this rock star status deserved? Will mirror neurons have the star power longevity of Mick Jagger? Or are they just back up singers?

The hidden mirror

So what exactly are mirror neurons? While studying neurons in motor areas of the frontal lobe of the Rhesus monkey brain, Rizzolatti's team noticed that some cells were responsive not only when the monkey performed an action, such as grasping a raisin, but also when the monkey simply watched the experimenter perform the same action. It was as if these neurons were simulating, or mirroring, a perceived action in the motor system of the animal. This is a very interesting and important finding, showing that sensory and motor systems interact in the brain's cortex at the single cell level.

But the interpretation of mirror neurons since then has extended well beyond sensory-motor interaction. For example, some have speculated that mirror neurons are the basis for our ability to understand the actions of others: because we know the consequences of our own actions, we can understand and anticipate the intended consequences of others' actions by activating similar neural networks in our own motor system. This concept was quickly generalized to more complex functions: because we speak, feel emotion, and have a sense of our own intentions, the theory goes, we can understand the speech of others, empathize, and "mind-read" intentions by mapping other people's behaviors onto our own mirror neuron system.

What is really being reflected?

Is the speculation that mirror neurons are responsible for "understanding" the behavior of others justified? Or are mirror neurons involved in less lofty, but nonetheless important, mental functions? A new study -- "Sensosirmotor Leaning Configures the Human Mirror System," from Current Biology (abstract or pdf download -- suggests the latter. Carolyn Catmur, Vincent Walsh, and Cecilia Heyes, researchers at University College London's Institute of Cognitive Science, stimulated the hand-related portions of motor cortex of human volunteers while they watched videos of hands performing movements of the index or little finger. Stimulation was accomplished using "transcranial magnetic stimulation" (or TMS), in which magnetic pulses are passed through the skull to induce brief electrical currents in the underlying brain tissue. TMS of motor cortex hand areas results in electrical neural impulses being transmitted to the hand itself, where these impulses can be measured by placing electrodes over the finger muscles. The researchers found that when a volunteer watched index finger movement, motor-cortex stimulation by TMS led to stronger electrical signals in the participant's own index finger compared to the pinky, and vice-versa when watching pinky finger movement. This is a mirror-neuron-like effect. Watching a video of index finger movement induces activation of the observer's own motor system controlling index finger movement. This naturally induced activity then sums with the TMS-induced activity to produce stronger than normal neural signals in the index finger muscles.

The mirror neuron theorists would say that our "understanding" of this movement is a result of this heightened activation of our own motor system. But Catmur and colleagues went beyond this basic mirror neuron result. After their initial measurements, they trained the participants to make "counter-mirror" movements: that is, when you see the index finger move, move your own pinky finger, and vice-versa. After this training, the brain responses were reassessed -- and a reversal of the mirror effect was found: watching index-finger movement resulted in more electrical activity in the pinky, and watching pinky movement produced more activity in the index finger. The brain learned new sensory-motor associations, and it is these associations that underlie the mirror neuron-like effect.

Fodder for, not parent of

This is a very nice demonstration that mirror system-like activity is subject to sensory-motor learning, suggesting it is learned rather than hard-wired. But the real question for the mirror neuron theory of action understanding is what these newly trained volunteers "understand" about these movements. Since viewing index finger movement induces activity in the participants' pinky motor systems, do they now think they are viewing little finger movement? Of course not. They still understand that they are viewing index finger movement. Conclusion: mirror system activation is not necessarily correlated with "understanding" but rather with sensory-motor learning.

This dissociation between mirror neuron-like activity and understanding comes as no real surprise. We know from decades (centuries even) of research involving patients with aphasia (language deficits resulting from brain damage, typically stroke) that it is possible to lose virtually all ability to articulate words while retaining the ability to understand the meaning of spoken words. Loss of the motor system controlling speech production, which contains the mirror system for speech, does not result in loss of the ability to understand the speech actions of others. It is also possible for the reverse situation to happen: in some patients with damage that spares the mirror system, the ability to repeat the speech of others may be intact (indicating intact sensory-motor associations), and yet they fail to understand the words. As in the study described above, mirror system function and action understanding dissociate.

The implications are clear. The mirror neuron system is not the neural basis for action understanding. This is true for simple limb actions of the sort that led to the discovery of mirror neurons in the monkey, and it is true for the first complex human behavior that the mirror neuron theory was generalized to, namely speech. If the mirror neuron theory shatters for these behaviors, its generalization to abilities like empathy or "mind-reading" seems ridiculously overstated.

This is not to say that a neural network supporting sensory-motor associations isn't important, or even that such associations are irrelevant to action understanding, language and the like. It seems quite likely that these higher-level systems make use of information derived from sensory-motor linkages. But that mirror neurons provide information that gets used by this high-level understanding does not mean that mirror neurons encode and produce this high-level understanding. You might be able to train a parrot to say "I can't get no satisfaction" -- but that doesn't mean he understands the message. Despite the hype to the contrary, mirror neurons are not the Mick Jagger of cognitive neuroscience. But there's no shame in singing backup. After all, who would want to sit through two hours of Mick singing a cappella? You need a whole band to make good music. The brain works the same way.

Gregory Hickok is professor of cognitive neuroscience and the director of the Center for Cognitive Neuroscience at the University of California, Irvine. He blogs on the neural underpinnings of language at Talking Brains and contributes to a UC Irvine cog-sci group blog as well.

Spoken-word processing in aphasia

from Brain and Language

Two studies were carried out to investigate the effects of presentation of primes showing partial (word-initial) or full overlap on processing of spoken target words. The first study investigated whether time compression would interfere with lexical processing so as to elicit aphasic-like performance in non-brain-damaged subjects. The second study was designed to compare effects of item overlap and item repetition in aphasic patients of different diagnostic types. Time compression did not interfere with lexical deactivation for the non-brain-damaged subjects. Furthermore, all aphasic patients showed immediate inhibition of co-activated candidates. These combined results show that deactivation is a fast process. Repetition effects, however, seem to arise only at the longer term in aphasic patients. Importantly, poor performance on diagnostic verbal STM tasks was shown to be related to lexical decision performance in both overlap and repetition conditions, which suggests a common underlying deficit.

Are regular and irregular verbs dissociated in non-fluent aphasia? A meta-analysis

Abstract

The cognitive mechanisms and neuroantomical substrates used by the brain to effortlessly generate morphologically complex words (write + ing → writing) are little understood. The left inferior frontal gyrus (LIFG, including Broca's area) is often implicated as being involved, although its specific role is unclear. Data from brain damaged individuals, particularly those with Broca's aphasia, are often used as evidence to support or refute various theoretical perspectives. Typically, performance on two types of morphologically complex verbs, regulars (walk-walked, slip-slipped) and irregulars (sing-sang, sleep-slept) is contrasted for evidence of single or double dissociations. The question of how Broca's aphasic individuals dissociate in their production of inflectional morphology is important to our understanding of how the brain is organized to compute morphologically complex words. This article is a synthesis of research studies investigating the production of morphologically complex regular and irregular verbs in individuals with Broca's aphasia. The question being asked is if there is a robust and consistent dissociation, and if this dissociation can be tied to lesions of the left frontal lobe. This meta-analysis of 75 patients failed to show a single consistent dissociation pattern and over half the datasets had no significant difference between regulars and irregulars. There was also no relationship of any performance pattern to frontal lobe lesions, highlighting the difficulty of identifying any single neuroanatomical lesion for regular–irregular verb production deficits. The implications for various theoretical and neuroanatomical hypotheses are discussed. The role of neuropsychological dissociations in constraining hypothesis of normal neuroanatomical organization is evaluated.


Keywords: Morphology; Broca's aphasia; Language production; Sentence completion; Repetition; Verb

Process skill rather than motor skill ..

... seems to be a predictor of costs for rehabilitation after a stroke in working age; a longitudinal study with a 1 year follow up post discharge

Ann Bjorkdahl email and Katharina S Sunnerhagen email

BMC Health Services Research 2007, 7:209doi:10.1186/1472-6963-7-209
Published: 21 December 2007
Abstract (provisional)

Background

In recent years a number of costs of stroke studies have been conducted based on incidence or prevalence and estimating costs at a given time. As there still is a need for a deeper understanding of factors influencing these costs the aim of this study was to calculate the direct and indirect costs in a "young" (<65) sample of stroke patients and to explore factors affecting the costs.

Information about Cerebrovascular Disease

By Robert Baird
January 16, 2008


The signs and symptoms of cerebrovascular disease depend on the location of the hemorrhage, thrombus, or embolus and the extent of cerebral tissue affected. General signs and symptoms of a hemorrhagic or ischemic event include motor dysfunction, such as hemiplegia and hemiparesis.

Early in a CVA, the patient may experience flaccid paralysis, followed by increased muscle tone and spasticity. He may lose his gag reflex and ability to cough. He may have communication deficits, such as dysphagia, receptive or expressive aphasia, dysarthria, and apraxia. He also may develop spatial and perceptual deficits, such as the loss of half of his visual field (homonymous hemianopia) and the inability to recognize an object (agnosia).

Other signs and symptoms of a CVA include vomiting, seizures, fever, ECG abnormalities, confusion that leads to a complete loss of consciousness, labored or irregular respirations, apneic periods, increased blood pressure, and bowel and bladder incontinence.

Signs and symptoms specific to a hemorrhagic CVA include abrupt onset of a severe headache, nuchal rigidity, and rapid onset of complete hemiplegia. As the hematoma enlarges, the patient's neurologic deficits worsen from gradual loss of consciousness to coma.

Signs and symptoms of a thrombotic CVA follow the "stroke in evolution" pattern and include the progressive deterioration of motor and sensory function, slow deterioration of speech, and lethargy. These signs and symptoms peak when edema develops, usually about 72 hours after the onset of the thrombotic event.

Next.........

The Mini-Mental State Examination in Behavioral Variant Frontotemporal Dementia and Primary Progressive Aphasia

The Mini-Mental State Examination in Behavioral Variant Frontotemporal Dementia and Primary Progressive Aphasia
Jason E. Osher, MS

Cognitive Neurology and Alzheimer's Disease Center, Nowrthwestern University Feinberg School of Medicine, Chicago, Illinois, Department of Psychiatry and Behavioral Sciences, Nowrthwestern Universtiy Feinberg School of Medicine, Chicago, Illinois, jason-osher@northwestern.edu

Alissa H. Wicklund, PhD

Cognitive Neurology and Alzheimer's Disease Center, Nowrthwestern University Feinberg School of Medicine, Chicago, Illinois

American Journal of Alzheimer's Disease and Other Dementias®, Vol. 22, No. 6, 468-473 (2008)
DOI: 10.1177/1533317507307173
© 2008 SAGE Publications

How left inferior frontal cortex participates in syntactic processing: Evidence from aphasia

from Brain and Language

We report on three experiments that provide a real-time processing perspective on the poor comprehension of Broca’s aphasic patients for non-canonically structured sentences. In the first experiment we presented sentences (via a Cross Modal Lexical Priming (CMLP) paradigm) to Broca’s patients at a normal rate of speech. Unlike the pattern found with unimpaired control participants, we observed a general slowing of lexical activation and a concomitant delay in the formation of syntactic dependencies involving “moved” constituents and empty elements. Our second experiment presented these same sentences at a slower rate of speech. In this circumstance, Broca’s patients formed syntactic dependencies as soon as they were structurally licensed (again, a different pattern from that demonstrated by the unimpaired control group). The third experiment used a sentence-picture matching paradigm to chart Broca’s comprehension for non-canonically structured sentences (presented at both normal and slow rates). Here we observed significantly better scores in the slow rate condition. We discuss these findings in terms of the functional commitment of the left anterior cortical region implicated in Broca’s aphasia and conclude that this region is crucially involved in the formation of syntactically-governed dependency relations, not because it supports knowledge of syntactic dependencies, but rather because it supports the real-time implementation of these specific representations by sustaining, at the least, a lexical activation rise-time parameter.