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In from the postcentral gyrus (areas 3 discount extra super cialis 100mg with visa, 1 cheap 100mg extra super cialis overnight delivery, 2); the former terminate pri- addition purchase extra super cialis 100 mg otc, and with time cheap extra super cialis 100mg fast delivery, these patients may exhibit features of an upper marily in laminae VI-IX discount 100 mg extra super cialis mastercard, while the latter end mainly in laminae IV and motor neuron lesion (hyperreflexia, spasticity, loss of superficial abdominal V. Prefrontal regions, especially area 6, and parietal areas 5 and 7 also reflexes, and the Babinski sign). Bilateral cervical spinal cord damage contribute to the corticospinal tract. Unilateral spinal cord lesions in thoracic levels may result in paral- ( ), and substance P ( , plus other peptides) are found in small cor- ysis of the ipsilateral lower extremity (monoplegia). If the thoracic spinal tical neurons presumed to function as local circuit cells or in cortico- cord damage is bilateral both lower extremities may be paralyzed (para- cortical connections. Small lesions within the decussation of the pyramids may result fibers that project to the spinal cord. Glutaminergic corticospinal fibers in a bilateral paresis of the upper extremities (lesion in rostral portions) and terminals are found in all spinal levels but are especially concen- or a bilateral paresis of the lower extremities (lesion in caudal portions) trated in cervical and lumbosacral enlargements. This correlates with based on the crossing patterns of fibers within the decussation. Some corticospinal dromes), or midbrain (the Weber syndrome) all produce alternating fibers may branch and terminate at multiple spinal levels. These present as a contralateral hemiplegia of the tor neurons are influenced by corticospinal fibers either directly or in- upper and lower extremities, coupled with an ipsilateral paralysis of directly via interneurons. Acetylcholine and calcitonin gene-related the tongue (medulla), facial muscles or lateral rectus muscle (pons), peptides are present in these large motor cells and in their endings in and most eye movements (midbrain). Lesions in the internal capsule (lacu- Clinical Correlations: Myasthenia gravis, a disease characterized nar strokes) produce contralateral hemiparesis sometimes coupled with by moderate to profound weakness of skeletal muscles, is caused by various cranial nerve signs due to corticonuclear (corticobulbar) fiber circulating antibodies that react with postsynaptic nicotinic acetyl- involvement. Bilateral weakness, indicative of corticospinal involve- choline receptors. Progressive muscle fatigability throughout the day ment, is also present in amyotrophic lateral sclerosis. Abbreviations ACSp Anterior corticospinal tract LCSp Lateral corticospinal tract Somatotopy of CSp Fibers ALS Anterolateral system ML Medial lemniscus A Position of fibers coursing to APGy Anterior paracentral gyrus MLF Medial longitudinal fasciculus upper extremity regions of BP Basilar pons PO Principal olivary nucleus spinal cord CC Crus cerebri PrCGy Precentral gyrus L Position of fibers coursing to CNu Corticonuclear (corticobulbar) Py Pyramid lower extremity regions of fibers RB Restiform body spinal cord CSp Corticospinal fibers RNu Red nucleus T Position of fibers coursing to IC Internal capsule SN Substantia nigra thoracic regions of spinal cord Review of Blood Supply to Corticospinal Fibers STRUCTURES ARTERIES Posterior Limb of IC lateral striate branches of middle cerebral (see Figure 5–38) Crus Cerebri in paramedian and short circumferential Midbrain branches of basilar and posterior communicating (see Figure 5–27) CSp in BP paramedian branches of basilar (see Figure 5–21) Py in Medulla anterior spinal (see Figure 5–14) LCSp in Spinal Cord penetrating branches of arterial vasocorona (leg fibers), branches of central artery (arm fibers) (See Figure 5–6) Motor Pathways 191 Corticospinal Tracts Thigh Somatomotor cortex Leg APGy Foot Somatotopy of CSp Post. These fibers influence—ei- lesioned side and away from the side of the hemiplegia. In addition to ther directly or through neurons in the immediately adjacent reticular a contralateral hemiplegia, common cranial nerve findings in capsular le- formation—the motor nuclei of oculomotor, trochlear, trigeminal, ab- sions may include 1) deviation of the tongue toward the side of the ducens, facial, glossopharyngeal and vagus (both via nucleus ambiguus), weakness and away from the side of the lesion when protruded and 2) spinal accessory, and hypoglossal nerves. This reflects the fact that corticonuclear (cortico- eas 6 and 8 in caudal portions of the middle frontal gyrus), the precen- bulbar) fibers to genioglossus motor neurons and to facial motor neu- tral gyrus (somatomotor cortex, area 4), and some originate from the rons serving the lower face are primarily crossed. Fibers from area 4 occupy the genu of ticonuclear fibers to the nucleus ambiguus may result in weakness of the internal capsule, but those from the frontal eye fields (areas 8,6) may palatal muscles contralateral to the lesion; the uvula will deviate to- traverse caudal portions of the anterior limb, and some (from areas wards the ipsilateral (lesioned) side on attempted phonation. In addi- 3,1,2), may occupy the most rostral portions of the posterior limb. In contrast to from area 4 terminate in, or adjacent to, cranial nerve motor nuclei ex- the alternating hemiplegia seen in some brainstem lesions, hemisphere cluding those of III, IV, and VI. In addition, it is important to note the following: 1) vertical gaze palsies (midbrain), 2) the Parinaud syn- that descending cortical fibers (many arising in areas 3, 1, 2) project to drome—paralysis of upward gaze (tumors in area of pineal), 3) internu- sensory relay nuclei of some cranial nerves and to other sensory relay clear ophthalmoplegia (lesion in MLF between motor nuclei of III and nuclei in the brainstem, such as those of the posterior column system. VI), 4) horizontal gaze palsies (lesion in PPRF), or 5) the one-and-a-half Neurotransmitters: Glutamate ( ) is found in many corticofu- syndrome. In the latter case, the lesion is adjacent to the midline and in- gal axons that directly innervate cranial nerve motor nuclei and in volves the abducens nucleus and adjacent PPRF, internuclear fibers those fibers that terminate near (indirect), but not in, the various mo- from the ipsilateral abducens that are crossing to enter the contralat- tor nuclei. The cerebral artery occlusion) or the internal capsule (as in lacunar strokes result is a loss of ipsilateral abduction (lateral rectus) and adduction or occlusion of lenticulostriate branches of M1) give rise to a con- (medial rectus, the “one”) and a contralateral loss of adduction (medial tralateral hemiplegia of the arm and leg (corticospinal fiber involve- rectus, the “half ”); the only remaining horizontal movement is con- ment) coupled with certain cranial nerve signs. Strictly cortical lesions tralateral abduction via the intact abducens motor neurons. Abbreviations AbdNu Abducens nucleus OcNu Oculomotor nucleus AccNu Accessory nucleus (spinal accessory nu. Many of brainstem and spinal cord, and the general distribution of tectospinal reticulospinal fibers influence the activity of lower motor neurons. Tectospinal fibers originate from deeper lay- Clinical Correlations: Isolated lesions of only tectospinal and ers of the superior colliculus, cross in the posterior (dorsal) tegmental reticulospinal fibers are essentially never seen. Tectospinal fibers pro- decussation, and distribute to cervical cord levels. Several regions of ject to upper cervical levels where they influence reflex movement of cerebral cortex (e. Such movements may be diminished or slowed in tum, but the most highly organized corticotectal projections arise from patients with damage to these fibers. Pontoreticulospinal fibers (medial reticulospinal) ulospinal) fibers are excitatory to extensor motor neurons and to neu- tend to be uncrossed, while those from the medulla (bulboreticu- rons innervating axial musculature; some of these fibers may also in- lospinal or lateral reticulospinal) are bilateral but with a pronounced hibit flexor motor neurons.

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These effects are consistent with the neurons being overstimulated and depolarised as a result of chronic neuroleptic dosing and so requiring to be hyperpolarised (inhibited) in order to become active cheap extra super cialis 100 mg otc. In a neuron from an untreated rat (c) discount extra super cialis 100mg, GABA produces the expected inhibition and glutamate the rapid excitation buy generic extra super cialis 100 mg online, shown as an oscilloscope sweep in (d) purchase extra super cialis 100 mg with mastercard. This again emphasises the importance of feedback loops in DA neuron function and schizophrenia as discussed above proven extra super cialis 100 mg. Second, although typical neuroleptics produce depolarisation block of both A9 and A10 neurons, the atypical neuroleptics only induce it in A10 neurons (Chiodi and Bunney 1983). So after an atypical neuroleptic the A9 neurons of the nigrostriatal tract remain functional, which would explain why EPSs are not seen. Another difference is seen with the expression of an immediate-early gene, c-fos, and although its functional significance is not clear, typical neuroleptics induce its protein production in both the striatum and nucleus accumbens while the atypicals only achieve it in the accumbens. The slow time-course of depolarisation block not only offers an explanation for the latency of action of neuroleptic drugs but its occurrence may explain how they actually reduce DA function. Whether it explains their antischizophrenic effect is less certain since it is not possible to determine if such depolarisation occurs in patients on neuro- leptic drugs. Certainly if this is how neuroleptics work it cannot be claimed that they have returned brain function to normal. SCHIZOPHRENIA 363 THE EXTRAPYRAMIDAL SIDE-EFFECTS (EPSs) OF NEUROLEPTIC DRUGS These take three basic forms (1) Acute dyskinesias (2) Parkinsonian-like symptoms, e. It is not surprising that a DA antagonist (especially those acting primarily on D2 receptors) should produce the symptoms of Parkinsonism, a disorder caused by inadequate DA function (see Chapter 15), nor that its intensity or rate of onset over some weeks or months should increase with D2 antagonistic potency. Tolerance to this adverse effect can develop without affecting antipsychotic activity but the speed with which Parkinsonism resolves after stopping therapy may be from 3 to 12months and can persist indefinitely in some cases. The late (tardive) dyskinesias, which mainly involve facial muscles, can take months or years to develop. They occur in 20±40% of patients, may not cease after stopping the drug and in fact can get worse, or even start then. Since they can be reduced temporarily by increasing neuroleptic dose it would appear that they do really result from DA overactivity and that the antagonism is not adequate. Certainly many experimental studies show that long-term neuroleptic dosing causes a compensatory increase in DA receptor number which would predispose to dyskinesias. Against this view are the findings that the increase in receptor number may precede dyskinesias by many weeks, receptor number but not dyskinesias routinely decline after drug withdrawal and while all patients should develop increased receptor number only some show dyskinesias. The dyskinesias are also more common in schizophrenics with clear negative symptoms and most brain damage and, since they have been seen in some untreated schizophrenics, could be a latent feature brought out by neuroleptics. Of course if the A9 neurons have been depolarised by the neuroleptics (see above) it is difficult to see how they can become so active unless the depolarisation also wears off. ATYPICAL NEUROLEPTICS Typical neuroleptics reduce the positive symptoms of schizophrenia at the expense of producing EPSs but the so-called atypical neuroleptics have less tendency to cause EPSs. Clozapine can even be effective in patients refractory to other neuroleptics. It is clearly a special drug, so special in fact that although it was once withdrawn because it causes agranulocytosis in some patients (2%), it has been reintroduced, alongside careful blood monitoring, for refractory cases. This has been shown by (1) increased DA turnover through DOPAC and HVA production in vitro, (2) augmented DA and DOPAC release by microdialysis in vivo and (3) increased c-fos-like expression. How the atypical neuroleptics achieve this differential effect is less clear but they could achieve some control of schizophrenia without producing EPSs by: (1) Acting primarily on a particular subset of DA receptors (2) Antagonising (or augmenting) some other NT(s) instead of, or in addition to, DA (3) Having a particular but appropriate profile of DA and other NT (antagonistic) effects These possibilities will be considered in turn. Significance of different DA receptors So far we have generally just alluded to the neuroleptics as DA receptor antagonists. Clearly, if the DA released at the terminals of one dopaminergic tract acted on a subset of DA receptors that were different from those found postsynaptically at other tracts then some specificity of antagonist action might be achieved. Unfortunately there is no evidence that different pathways innervate different DA receptor populations and as with the use of agonists in PD, the D2 receptor is dominant. Specific D1 antagonists have no anti- schizophrenic effect and antischizophrenic efficacy increases with neuroleptic affinity (potency) at D2 receptors Ð as unfortunately does the tendency to produce EPSs. Thus there is no great advantage in producing more potent D2 antagonists, other than that less drug needs to be incorporated into long-term release depot preparations. PET studies show that at effective therapeutic plasma concentrations most neuro- leptics occupy some 80% of brain D2 receptors (in the striatum at least) and this is therefore considered to be a requirement for efficacy (Pilowsky, Costa and Eli 1992; Farde 1996). If that is so then clozapine, which occupies only 20±40% of the D2 receptors at a therapeutic concentration, must have some other action which accounts for its therapeutic effectiveness. Its activity at D1 receptors has been put forward as a possibility and although it has a relatively higher affinity for D1 than D2 receptors, compared with typical neuroleptics, it is still a weak antagonist at both and in the absence of evidence for D1 (or D5) receptor involvement in schizophrenia the significance of any D1 antagonism is unclear.

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The seizure Individuals may pace extra super cialis 100 mg low cost, wander aimlessly discount extra super cialis 100mg fast delivery, generally lasts for only seconds cheap extra super cialis 100 mg. The indi- make purposeless movements cheap 100 mg extra super cialis visa, and utter vidual does not fall 100 mg extra super cialis visa, and there are usual- unintelligible sounds. The seizure can last ly no outward motor manifestations of up to 20 minutes, with mental confusion absence seizures, although abnormal lasting for a few minutes after the seizure blinking or slight twitching may occur is over. Because of the limited visi- toms of complex-partial seizures, often ble symptoms of the seizure, those around attributing the symptoms to alcohol, the individual may misinterpret absence drug abuse, or mental illness. When children experience frequent Status Epilepticus absence seizures, school performance may be disrupted. Because there may be no Status epilepticus is a term used to de- significant signs that are easily observed scribe seizures that are prolonged or that during the seizure, the seizure disorder come in rapid succession without full re- may not be diagnosed, and poor school covery of consciousness between seizures. Recognition of symptoms and life–threatening and consequently re- appropriate diagnosis are crucial to enable quires immediate medical attention and children to achieve maximum school treatment (Lowenstein & Alldredge, 1998). Absence seizures may disappear spontaneously with age, although some Diagnosis of Epilepsy individuals who have had absence seizures later go on to develop tonic-clonic seizures. Individuals who are having a seizure for the first time usually undergo medical Partial Seizures evaluation by a neurologist to determine whether the seizure is a symptom of an When nerve cells discharge in an isolat- acute medical or neurological illness that ed part of the brain, partial seizures occur. Exten- and symptoms are very localized, depend- sive physical examination and blood tests ing on the part of the brain affected. One are usually part of initial screening, as well type of focal seizure, a Jacksonian (simple- as a detailed history of the precipitating partial) seizure, begins with convulsive factors that appeared to trigger the seizure. The convulsive muscle seizure, or when other symptoms or his- Conditions Affecting the Brain 63 tory indicate that epilepsy may be the nausea, dizziness, clumsiness, visual diffi- cause of seizure activity, a more extensive culty, or fatigue. A pri- Once medication for treatment of mary diagnostic tool for evaluating indi- seizures has begun, it is generally main- viduals after seizures is electroencephalo- tained for at least two years, regardless of graphy (EEG), a noninvasive procedure in whether the individual has remained which the electrical activity of the brain seizure free (Browne & Holmes, 2001). Magnetic resonance there have been no recurrent seizures after imaging (MRI), a noninvasive procedure in this time, the physician may consider which rapid detailed pictures of body withdrawing the medication. Individuals structures are produced, may also be used who have had no additional seizures after to identify structural anomalies in the beginning the medication, or who have brain that may be related to seizures. Treatment and Management of Epilepsy The consequences could be dangerous and at times life-threatening. Consequently, Treatment of epilepsy is dependent on the individuals should never attempt to alter cause of the seizure activity and the types or discontinue their medication without of seizures experienced. Al- the type of seizure and on whether more though they may be thoroughly evaluat- than one type of seizure is experienced. Based tion to remove or repair the abnormality on medication blood level and its effec- may be indicated. In most instances, how- tiveness in controlling seizure activity, the ever, when epilepsy is diagnosed, the stan- physician may alter medication dosages dard treatment of most types of seizures accordingly. Measuring the blood levels of is the regular use of one or more anticon- the anticonvulsant also helps the physi- vulsant or antiepileptic medications. Successful con- compliant with taking anticonvulsant med- trol of seizures, however, requires the indi- ications, seizures remain uncontrolled. The anticonvul- several seizures a month or, at times, sev- sant medications used to treat epilepsy are eral seizures a day, despite following a also not without side effects, and toxic strict treatment regimen of medication. Depending on the medication, cannot be controlled by medication, sur- side effects can include gum overgrowth, gery may be recommended to treat epilep- 64 CHAPTER 2 CONDITIONS OF THE NERVOUS SYSTEM: PART I sy. Under these circumstances, surgery well controlled seizures are, individuals may involve removing a portion of the live with the possibility, even if remote, brain structure, resecting a portion of the that another seizure will occur. The time, brain, or disconnecting the affected por- place, and social circumstances under tion from the rest of the brain. The amount If individuals experience a seizure in pub- of disability experienced, if any, after this lic, they risk feelings of embarrassment type of surgery depends on individual cir- and onlookers’ potential misperception of cumstances. Alcohol can lower the seizure threshold At times, even when seizures are adequate- and therefore precipitate seizures. Alcohol ly controlled, anxiety over the possibility and antiepileptic medications may also of having a seizure or other psychosocial interact and cause untoward effects. Con- dysfunction may be the most disabling sequently, individuals with epilepsy should factor associated with the condition. A medical ment and emotional development depend identification bracelet should be worn by on when the diagnosis of epilepsy is made individuals with epilepsy at all times. When epilepsy is diagnosed in child- with epilepsy depends on the type of hood, parental feelings of fear, anxiety, seizure, the underlying cause, the admin- guilt, overprotectiveness, or mourning istration of appropriate treatment, and the can affect not only the child’s ability to individual’s willingness and ability to fol- accept his or her disability but also his or low the prescribed treatment regimen.

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Although there is some comfort in the fact that few cases involve physician incompetence or technical inadequacy order 100mg extra super cialis amex, this is no solace to the patient and does not form the basis of a strong defense in court purchase 100 mg extra super cialis fast delivery. The vast majority of cases allege delay in diagnosis buy extra super cialis 100mg low cost, and these claims may be divided into those involving diagnostic error and those involving poor communication cheap extra super cialis 100 mg visa. Additional claims arise from therapeutic acts of omis- sion or commission purchase extra super cialis 100 mg amex. Breast cancer is a common disease, and most women are familiar with the cumulative incidence figure that one in nine American women will have breast cancer in her lifetime. Although this figure is accu- rate, it is somewhat misleading because it includes precursor in situ lesions that have not yet become cancers and assumes that women will live to age 80 years or older and not die from other causes before that age. The prevalence of the disease is increasing because of the wide use of mammographic screening and the aging of the population (the incidence rises with age). Most breast cancers present without symp- toms, and it is the patient herself who most often discovers the tumor; therefore, any delay in diagnosis is both readily apparent and unlikely to be excused. The Doctors Company (TDC), a national physician-owned medical malpractice insurance company, analyzed 100 closed claims involving breast cancer in an attempt to identify repetitive problems (2–4). This is, to our knowledge, the largest single-source breast cancer claims study ever undertaken. Closed claims were reviewed to ensure the full range Chapter 12 / Breast Cancer Litigation 155 of outcome data would be available. Consecutive files were chosen to evaluate all actual case presentations independent of outcome. Overall Outcomes The 100 consecutive files involved 80 individual patients with breast cancer. In these cases, 127 physicians were defendants and 42 (33%) ultimately paid indemnity. Of the 80 women, 36 (45%) were successful against at least one defendant physician. Four claims went to trial and two resulted in a verdict for the plaintiff. Presenting Symptoms Clinical findings on presentation were documented in 71 cases. A palpable lump was found in 28 cases, pain was present in 8 cases, and there was nipple discharge in 1 case. Discovery of the Mass Frequently, the patient discovers her own breast cancer. In this series, the patient made the initial finding of a mass in 33 of 46 (72%) cases where the initial discovery was clearly documented. In the 13 cases where the physician initially detected the mass, the average indemnity was $156,538. Overall, TDC closes more than 80% of its claims without any indem- nity payment (5). When cases go to trial, TDC gains a defense verdict four of of five times. In this study, indemnity was paid on behalf of the defendant physician 33% of the time, and overall, 45% of breast cancer plaintiffs received payment from at least one physician defendant. The fact that the patient herself so frequently discovers the mass is an important part of the reason for this difference, because any delay in the ultimate diagnosis of cancer is apparent. Moreover, it is the patient herself who has brought the problem to the physician’s attention, so it is difficult to excuse unnecessary delay. Therefore, it is not surpris- ing that indemnity payments are considerably higher where the patient rather than the doctor initially detects the tumor ($350,000 vs $156,538). When the physician discovers the tumor, it is more likely that the patient has contributed to any delay in diagnosis. Physician Specialties Doctors in nearly all specialties see patients with breast cancer, but the litigation burden falls most heavily on those charged with making 156 Anderson and Troxel Fig. Radiologists who read the mammograms, patholo- gists who read the biopsies, and obstetricians/gynecologists who fre- quently provide primary care for women are the specialists most frequently sued (see Fig. Mammography It appears that many patients believe that screening mammography should either prevent the disease or guarantee a cure if it is found. The likelihood that an individual screening mammogram will reveal malig- nancy is between 1 in 200 and 1 in 250 (5a). This makes finding the one true positive study difficult, but gives patients an exaggerated sense of the protective effect of screening. Mammograms are involved in the majority of breast cancer cases and are the most common source of malpractice claims against radi- ologists.

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