Actually, it can be all of them, but the most frequent cause of acute uncompensated respiratory acidosis in a young person is bronchopneumonia.

A 40-year-old male, foreign tourist, is referred to the ED for low level of consciousness, temperature of 37.7°C and dyspnea. He has no trauma. Several tests were performed. The most immediate is an ABE without oxygen, showing PH 7.33, PCO2 50, PO2 65, HCO3 27:

Using 99mTc-DTPA radioaerosol inhalation lung scan as compared with computed tomography to detect lung injury in blunt chest trauma.

Detection of pulmonary contusion in patients with blunt chest trauma is very important so as to commence therapy immediately to avoid irreversible damage. The purpose of our study was to evaluate the efficacy of technetium-99m diethylene triamine pentaacetic acid (99mTc-DTPA) aerosol inhalation lung scintigraphy in comparison with chest computed tomography (CT) in the diagnosis of pulmonary contusion at acute blunt chest trauma. Twenty-nine patients with isolated blunt chest trauma were referred to the emergency department of our hospital, and nine healthy people participated in this study. Sixteen patients who had pulmonary contusion on CT scans were referred to as group 1, and 13 patients who had normal CT scans as group 2. Nine healthy people comprised a control group. 99mTc-DTPA aerosol inhalation lung scintigraphy was performed on the first day in all patients. The mean half time (T1/2) and penetration index values of 99mTc-DTPA clearance were significantly lower in groups 1 and 2 compared with the control group. Among the three groups, there were no significant differences in arterial blood gas analysis except for PO2. The mean T1/2 value of 99mTc-DTPA clearance did correlate with PO2 values but not with pH, PCO2, or HCO3 values. 99mTc-DTPA radioaerosol inhalation lung imaging may serve as a useful adjunct and supportive method to chest CT scanning for detecting mild pulmonary contusion.

Amphetamine toxicity masked by concomitant γ-hydroxybutyrate (GHB) ingestion.

We report a case of a young male with amphetamine toxicity initially obscured by concomitant use of gamma-hydroxybutyrate (GHB), and the sympathomimetic symptoms emerged after GHB's effects receded. A 24-year-old unconscious man presented to emergency department showed the following vital signs upon admission: blood pressure 136/58 mmHg; heart rate 79 bpm; SpO2 87% under ambient air; body temperature 36.1 °C; Glasgow Coma Scale score 3. The pupils were not dilated. Arterial blood gas test revealed respiratory acidosis (pH = 7.229, pCO2 = 64.4 mmHg, pO2 = 42.3 mmHg, HCO3 = 26.3 mmol/L). Intubation was performed and the patient was transferred to intensive care unit. The patient regained consciousness and became agitated in association with sinus tachycardia (heartrate 143 bpm; blood pressure 173/61 mmHg). A few hours later, he experienced abrupt desaturation (SpO2 65%) and profuse, pinkish, frothy sputum. Chest radiography revealed a bat-wing perihilar shadowing, and computed tomography showed bilateral ground-glass opacity and an alveolar pattern from acute pulmonary edema. A high dose of benzodiazepine with a midazolam pump at 50 mg/h was administered to relieve symptoms. The patient's friends confessed to concomitant use of amphetamine and GHB. The urine toxicology result was positive for amphetamine (≧500 ng/mL). The patient improved later and was extubated at 4 days after the mitigation of pneumonia and discharged uneventfully 8 days later. In our patient, amphetamine intoxication was initially masked by concomitant use of GHB but appeared as GHB's effect attenuated. We wish to remind clinicians of variable clinical presentations of polydrug abuse.

[Intra-alveolar hemorrhage. An uncommon accident in a breath holding diver].

To date, pulmonary oedema in breath hold divers has only been reported after dives below 50 meters, hypoxaemic syncope being the most common risk. We recently observed a 35-year-old well-trained breath hold diver who was unable to achieve deep inspiration during a high-level competition. After two hours of repeated dives to a depth of 25 meters for approximately 2-minute periods with intermittent recovery the patient developed cough and haemoptysis. The chest X-ray revealed lung images suggestive of intra-alveolar haemorrhage. The patient had taken 1 g of aspirin per os for three days prior to diving. Symptoms subsided spontaneously in 48 hours and one month later all haematology tests were normal except for minimal alteration of platelet aggregation. Pulmonary oedema in breath hold divers is usually attributed to blood shift to the pulmonary circulation related to the lowered intra-thoracic pressure. In our case, oedema was secondary to intra-alveolar haemorrhage favoured by aspirin which should be avoided before breath hold diving.

[Changes in Po2, Pco2, pH, and HCO3 concentration and flow rates in human parotid saliva by tongue sour stimulation at various intervals].

The PO2, PCO2, pH, and HCO3- concentration and flow rates of parotid saliva were observed by tongue stimulation with 3% tartaric acid at various intervals in a human subject after about a one hour rest. The PO2, PCO2, pH, and HCO3- concentrations in parotid saliva were measured with a Blood Gas Analyzer System. The results are summarized as follows: 1) The mean PO2 and PCO2 of parotid saliva immediately before tongue stimulation were about 40 mmHg (range 33-44 mmHg) and 45 mmHg (41-48). There values were similar to those of venous blood. 2) PO2 increased to about 50 mmHg (46-54) 5 to 10 sec. after stimulation, and then 3 to 8 min. later, it decreased to a minimum value of about 28 mmHg (26-29) before returning to the resting level 15 min. after stimulation, when the intervals between stimulations were longer than 2 min., similar changes in PO2 were observed, whereas stimulations every 30 sec. or 1 min. had no effect on PO2. 3) PCO2 increased to about 98 mmHg (85-120) from the resting level of 45 mmHg (41-48) 5 to 10 sec. after stimulation, and returned to the resting level 1 min. after stimulation. When the intervals between stimulations were shorter than 20 min., the peak value of PCO2 by the first stimulation was higher than those induced by the following stimulations. When the interval was 30 sec. or 1 min., only the peak after the first stimulation was observed. 4) The pH of parotid saliva was about 7.4 (7.35-7.5) 30 to 50 sec. after stimulation, and it decreased below 6.5 about 12 min. after stimulation. When the interval between stimulations was 5 min., the pH of the parotid saliva after stimulation was always above 6.5. When the interval between stimulations was 1 min. or 30 sec., it remained at about 7.5. 5) The HCO3- concentration in parotid saliva depends almost exclusively on the pH when Pco2 remained unchanged. When Pco2 was high, however, the HCO3- concentration was affected by the change in Pco2. 6) There was no relationship between changes in the flow rate of parotid saliva and Po2, Pco2, pH, and the HCO3- concentration. Particularly, when the interval between stimulations was shorter than 5 min., the changes in flow rate had no effect on Po2, Pco2, pH, and the HCO3- concentration.

[A case of traumatic pneumatocele revealed by CT 36 years after blunt chest trauma].

An 82-year-old male farmer who came to our clinic in November 2004 had an abnormal mass shadow of soft tissue density in the left lower lobe on his chest radiography. He had once received sudden blunt chest trauma to his left anterior chest wall by heavy farm equipment and this had produced a relative large pulmonary laceration on the basal segment near aorta at age 47 in 1970. One month after the accident, he went to a local hospital for chest radiographic examination. Initially tuberculosis was suspected, but was denied after one year. In 1972 when he was 61-years-old, he had consulted our clinic on the first vivit, for evaluation the findings of the thin-walled parenchymal dead space with air-fluid level at the left basal segment which was confused with pleural effusion for a long time. Needle aspiration performed to the dead space yielded, whitish turbid fluid without tubercule bacillus was obtained. In November 2006, when he was 84-years-old, he again came to our clinic. By chest CT, the abnormal shadow was disclosed as a relatively large unilocular traumatic paneumatocele, 4 x 7cm in size, with an air-fluid level, encircled by a thick wall with noticeable calcification, located in the basal segment of the entirely collapsed lower lobe. From the findings of leucocytes are still found in the fluid of the site of laceration, and both elevation of CRP and the blood sedimentation rate, persistent inflammatory reaction in the lacerated space was suspected. We report a rare case in which a traumatic pneumatocele existed for 36 years. This case suggests the importance of chest CT in the diagnostic procedure of traumatic pneumatocele.

Long-term submergence at 3 degrees C of the turtle Chrysemys picta bellii in normoxic and severely hypoxic water. III. Effects of changes in ambient PO2 and subsequent air breathing.

Western Painted Turtles, Chrysemys picta bellii (N = 5), were maintained submerged and apneic for 90 days: days 0-21 in severely hypoxic water (PO2 = 0-5 mmHg), days 22-43 in aerated water (PO2 approximately 160 mmHg), and days 44-90 again in hypoxic water. From day 90 onward, the water was aerated and the turtles were allowed access to the air; water and air temperatures were maintained at 3 degrees C. Arterial blood samples were taken periodically and analysed for PO2, PCO2, pH, [Na+], [K+] [Cl-], [lactate-], [glucose] and haematocrit. Plasma [HCO3-] was calculated for all samples and total plasma calcium was measured on samples from two animals. Each exposure to low PO2 water caused progressive lactic acidosis and a transient respiratory acidosis with an accompanying fall in plasma [Cl-] and rise in plasma [K+] and [calcium]. During the intervening period in aerated water, blood pH recovered significantly (from 7.33 to 7.74 in 7 days), due primarily to a fall in PCO2 (from 23.5 to 10.6 mmHg), while [lactate-] remained unchanged (at about 50 mM), and [HCO-3] rose slightly. Plasma [K+] promptly returned to nearly normal values. When permitted to breathe on day 90, the three surviving turtles rapidly restored pH to normal by pronounced hyperventilation (PCO2 less than 5 mmHg). Metabolic acidosis, however, disappeared slowly with a t1/2 for [lactate-] and [HCO-3] restoration of about 2 weeks. We conclude that a wintering turtle can stabilize or even slightly improve its acid-base and ionic status by moving from an anoxic environment to well-oxygenated water. Further improvements can be gained by breathing air, but recovery proceeds at a very slow rate if the animal remains at 3 degrees C.

[Examinations to phenomenon of shock-lung (author's transl)].

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.

Phosgene exposure: a case of accidental industrial exposure.

Phosgene is a rare exposure with strong clinical implications. We report a phosgene exposure that resulted in the patient's death. A 58 year-old man arrived to the emergency department 1 hour after exposure to phosgene with complaints of a sore throat. Initial vital signs were blood pressure 175/118 mmHg, heart rate 98/min, respirations 12/min, and oxygen saturation of 93% on room air. Physical exam revealed few scattered rhonchi, without signs of distress. Initial arterial blood gases (ABG's) revealed pH 7.42, pCO2 43 mmHg, pO2 68 mmHg, HCO3 27 meq/L, and oxygen saturation of 93% on room air. Initial chest x-ray 2 hours after the exposure demonstrated clear lung fields. Approximately 2.5 hours after the exposure, he began complaining of dyspnea, restlessness and his oxygen saturation dropped below 90%. He received nebulized albuterol, 1 gram intravenous methylprednisolone, and 100 % oxygen via face mask. Minimal improvement was noted and he was intubated. The post intubation chest x-ray, 3.5 hours after the exposure, revealed diffuse alveolar infiltrates. Acetylcysteine, terbutaline, and IV steroids were administered without improvement. The patient died 30 hours after exposure. There are many misunderstandings concerning phosgene due to its rare presentation. Traditional treatment modalities are often unproven in human trials and were unsuccessful in this case. This case highlights the significant toxicity that results from phosgene exposure and the challenges of the limited treatment modalities. There is concern for the use of this agent in chemical terrorism.

[Bronchiolitis obliterans with idiopathic organizing pneumonia. Usefulness and yield of diagnostic techniques and procedures in a series of 20 patients].

To assess retrospectively the utility and the profitableness of the diagnostic procedures and techniques in patients with idiopathic BOOP. We studied epidemiological features, clinical manifestations, respiratory function tests, chest radiology, and other diagnostic procedures and techniques, as well as the evolution and the mortality rates in patients with histological diagnosis of idiopathic BOOP during the period 1992-1999. 20 patients (55% F, 45% M). Age: 64 +/- 15 years old, 50% smokers. The mean period elapsed since the beginning of the symptoms and the time of diagnosis was 51 +/- 30 days. The clinical presentation is of a subacute influenza-like illness, with fever, cough, dyspnea and crackles. The more common abnormalities were. WBC (10,949 +/- 2,6429 mm3, ESR 85 +/- 86 UI/L, LDH 309 +/- 86 UI/L. Arterial blood gas: PaO2 64 +/- 9, PaCO2 35 +/- 3 mmHg. Pulmonary function tests: VCF 81 +/- 25%, FEV1/VCF 78 +/- 17%, TLCO 74 +/- 9%, TLCO sb 77 +/- 4%. Radiological evaluation: bilateral multiple patchy alveolar opacities 75%), solitary focal lesion (15%) and interstitial opacities (10%). The bronchoscopy and BAL 10/20 (50%). Transbronchial biopsy 12/20 wit diagnosis (60%). The video assisted thoracoscopic lung biopsy 1/20 (5%) and open lung biopsy 7/20 (35%). Recurrences 8/20 (40%). Mortality rate 3/20 (15%). The idiopathic BOOP is a benign entity clinic inespecific, associated to hypoxemia and bilateral alveolar opacities. The transbronchial biopsy is a diagnostic procedure alternative to the open lung biopsy, in a compatible clínico-radiological context. The response to treatment is acceptable although it presents frequent exacerbations, and low mortality rate.

Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.

Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. Continuous monitoring of cerebrospinal fluid (CSF) pH, PCO2, HCO3-, base excess (BE), PO2, SO2, temperature, lactate and pyruvate (La and Py) measurements were conducted in 8 patients with severe head injury. Temperature-corrected CSF parameters were correlated with those in the jugular blood including oxygen saturation (SjO2), regional oxygen saturation (rSO2), intracranial pressure (ICP) and cerebral perfusion pressure (CPP), jugular blood temperature (Tjb), and endtidal PCO2 (PetCO2). Therapeutic significance of hyperventilation and hypothermia was evaluated. 1) CSF acidosis was observed in all cases (minimum pH 6.59-7.17) due to increased CSF PCO2 and/or decreased CSF HCO3- and tended to associate with abnormal ICP and/or CPP or ischemic episodes indicated by CSF PO2 and SO2, rSO2, and/or SjO2 during monitoring. 2) It was more obvious in CSF than in jugular blood that increased PCO2, La and Py, and/or decreased HCO3- resulted in decreased BE and pH. 3) Decreased CSF PO2 and SO2 only correlated with severe CSF acidosis. 4) Hyperventilation: Decreased PetCO2 did not always closely correlate with CSF PCO2 decrease and CSFpH increase. 5) Hypothermia: There were negative correlations of Tjb with CSF pH and SO2 in all cases, though correlation coefficients were not always high. CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. Hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.

[Preflight assessment by hypoxic inhalation test in cardiopulmonary patients].

Flying may expose passengers to hypoxic conditions, which may induce hypoxemia, particularly in those with chronic heart and/or lung disease. Onset of dyspnea, wheezing, chest pain, cyanosis and right heart failure can lead to urgent need for oxygen during flight. The hypoxia inhalation test (HIT) provides a safe and simple means of identifying those who may develop hypoxemia during flight. We report our experience with 48 self-reporting patients who underwent HIT prior to pre-planned air travel. They inhaled for 15-minute periods a reduced oxygen concentration (F1O2 15%) under normobaric conditions, during which O2 saturation was monitored by pulse oximeter; electrocardiogram, blood pressure and symptoms were also monitored. O2 saturation of < 85% (PaO2 50 mm Hg) was considered a positive test. In the 8 cases (17%) with a positive test, 5 had chronic obstructive pulmonary disease and 3 had cardiovascular and/or combined heart-lung disease. We calculated predicted O2 partial pressure in altitude (PaO2ALT) and compared it to actual results in the 8 patients with a positive HIT. In 5, use of the predicted formula would have under-diagnosed the hypoxemia that developed during the HIT. Thus, the results of the HIT changed treatment strategy in these patients. We recommend that patients with positive tests use O2 (2LPM or 4LPM) during flight. HIT is practical and of potential benefit in the objective assessment of patients with various degrees of heart, lung or combined heart-lung disease. Clinicians should be aware of the relative risk of hypoxia during flight in such patients, and of the value of HIT in identifying them, leading to increase in its use.

Mystery in the basement.

56 year-old male presented to the University of Mississippi Medical Center emergency department (ED) with complaints of progressive shortness of breath, productive cough, fever, and malaise. His past medical history was significant for hypertension as well as a 60 pack-year history of smoking. Upon arrival to the ED he had a temperature of 103.6 degrees F, blood pressure of 80/40 mm Hg, a pulse of 110 beats per minute, respirations of 28 per minute, and an oxygen saturation of 50% on room air. He appeared to be in significant respiratory distress. Lung examination revealed diffuse bilateral rhonchi and wheezes in all lung fields. He was emergently intubated. Chest radiograph demonstrated a miliary pattern scattered throughout all lung fields in addition to parenchymal opacities. A complete blood count revealed a white blood cell count of 33,500 10(3)/microL, hematocrit of 37%, and platelets of 906,000 10(3)/uL. Blood urea nitrogen and creatinine were 27 mg/dL and 1.0 mg/dL, respectively. Initial ABG on 100% oxygen showed pH 7.15, pCO2 82 mm Hg, and pO2 62 mm Hg. Troponin I was negative. An electrocardiogram demonstrated sinus tachycardia. Blood and urine cultures were obtained.

[Fire-eater's lung. Two cases and review of the literature].

Two men were hospitalized (three years apart) after aspirating petroleum on their fist attempt at "fire-eating". Pt.1 (aged 25 years) complained of chest pain, dyspnea and dizziness. The other (Pt. 2; aged 29 years) had a hemoptysis. Pt. 1 had a normal body temperature, but the breath sounds were decreased over the left base. The breath sounds in Pt. 2 were normal, but he had a fever of 38.8 degrees C. Routine physical examination was unremarkable. Laboratory tests in both patients revealed increased inflammatory parameters. Chest radiographs showed that Pt. 1 had a left basal alveolar infiltrate, while Pt. 2 had an infiltrate in the right middle and upper lobe, which on computed tomography after a few days showed signs of cavitation in the left infrahilar region and the middle lobe, respectively. Pneumococci were found in the sputum of Pt. 2. Both patients were given antibiotics, Pt. 1 also had salbutamol inhalation treatment. The patients were discharged symptom-free after 8 and 10 days, respectively. A follow-up chest radiograph four weeks later in Pt. 1 merely showed streaky-fibrotic residues. These two case reports and detailed literature search indicate that immediate administration of antibiotics is important, while routine steroid treatment is not necessary.

Oxygen status algorithm, version 3, with some applications.

The Oxygen Status Algorithm is a computer program which uses measurements from a pH & blood gas analyser and a hemoximeter to calculate the oxygen status and the acid-base status of the arterial blood. Version 3 features on-line data collection from the analyser; storage of up to 2000 patient cases in a Lotus 123 file format; printing of a Cumulated Patient Report in addition to the Patient Status Report; combination of arterial and mixed venous data for calculation of the shunt and the oxygen consumption rate (when cardiac output is keyed in); calculation of reference values for fetal haemoglobin for newborns (when gestational age is keyed in). Examples of applications answer the following questions: 1) Does hyperventilation improve the oxygen supply to the tissues? No, for a normal person a slight hypoventilation with a pCO2 of 8.5 kPa provides a maximal oxygen extraction tension. 2) What is the optimal hyperventilation at the top of Mt. Everest (ambient pressure 33 kPa)? Hyperventilation to a pCO2 of about 1.4 kPa provides a maximal oxygen extraction tension of 2.4 kPa for an unacclimatized person. 3) Which change in haemoglobin oxygen affinity would be equivalent to a decrease in arterial pO2 to 6.3 kPa? The oxygen extraction tension would decrease to 4.0 kPa and the same value would be caused by a decrease in half-saturation tension to 2.8 kPa, a decrease which could be due to a moderate alkalaemia (pH = 7.54) combined with a moderately decreased 2,3-diphosphoglycerate concentration (3.4 mmol/L). 4) Is temperature correction of the measured pO2 and pCO2 to the actual body temperature needed? Yes, for example, omitting temperature correction even when the patient temperature is only slightly decreased to 36 degrees C would result in a negative value for the calculated arterio-venous shunt fraction when the actual value, using temperature correction, is 11%. 5) Does the alpha-stat approach of pCO2 and pH regulation in hypothermia, where pH is allowed to rise as in blood in vitro, cause a fall in mixed venous pO2 below the critical value? No, although the mixed venous pO2 will be lower than with the pH-stat approach (constant pH at body temperature), it remains above the critical mixed venous pO2 level. The program is intended for clinical routine use as well as teaching purposes. It has context sensitive help as well as an extensive help index. A number of "demo" cases are provided with annotations in a separate file.

[The significance of maximal expiratory concentrations of CO2 (MEC CO2) in the negative diagnosis of acute pulmonary embolism in chronic obstructive bronchopneumopathies].

The aim of this prospective study was to analyse the contribution of the measurement of alveolar arterial gradients of CO2 during forced expiration in the diagnosis of pulmonary emboli occurring in chronic airflow obstruction (COPD) as a result of smoking. The study was carried out on 178 patients: Group 1: 54 subjects without emboli (14 controls, 33 COPD and 7 patients with chest pain); Group 2: 72 patients with proved emboli (49 non COPD, 23 COPD); Group 3: 52 patients COPD presenting with varied non-embolic broncho-pulmonary pathology (pneumonia, bronchospasm, pulmonary oedema, bronchial neoplasm). The diagnosis of pulmonary emboli was confirmed by scintigraphy in patients with non COPD or angiography (in patients with COPD). The maximal fraction of CO2 was measured using a capnologue during a forced expiration which was long and prolonged until residual volume was achieved. The PaCO2 was measured simultaneously by an analysis of arterial blood gases. The D index was calculated according to the formula [(PaCO2-PEM CO2)/PaCO2] x 100. The D index was significantly lower in Group 1 (3.42 +/- 3.8% p < 0.0001) than in Group 2 (20.8 +/- 10%) and Group 3 (17.6 +/- 11.7%) (not significant between Groups 2 and 3). In patients with COPD the specificity and sensitivity and the predicted positive and negative value were 100% for a D limit of 7%. In COPD patients these values were respectively 82, 95, 75 and 96% for a D limit of 7%; on the other hand for a D below 5% the values were 60, 100, 64 and 100% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxia (medical)

Hypoxia exists when there is a reduced amount of oxygen in the tissues of the body. Hypoxemia refers to a reduction in PO2 below the normal range, regardless of whether gas exchange is impaired in the lung, CaO2 is adequate, or tissue hypoxia exists. There are several potential physiologic mechanisms for hypoxemia, but in patients with COPD the predominant one is V/Q mismatching, with or without alveolar hypoventilation, as indicated by PaCO2. Hypoxemia caused by V/Q mismatching as seen in COPD is relatively easy to correct, so that only comparatively small amounts of supplemental oxygen (less than 3 L/min for the majority of patients) are required for LTOT. Although hypoxemia normally stimulates ventilation and produces dyspnea, these phenomena and the other symptoms and signs of hypoxia are sufficiently variable in patients with COPD as to be of limited value in patient assessment. Chronic alveolar hypoxia is the main factor leading to development of cor pulmonale—right ventricular

[Traumatic respiratory distress syndrome on plateau: diagnosis and treatment].

Twenty-seven adult patients, living at plateau, developed acute respiratory syndrome after severe trauma or major operation, were reported. Seven of them died. The clinical pictures were also of severe air-hunger, cyanosis and hypoxemia associated with diffusive interstitial edema of lungs, while the mean values of blood gases were much less compared with those of patients on plain, being P-a O2 33 mm Hg, Sat. O2 71%, PaCO2 31 mmHg, A-aDO2 426 mm Hg. The diagnostic points of ARDS of patient on plateau have been suggested and the urgent requirement of management for these patients on plateau has been emphasized and described.

Successful management of drug-induced hypercapnic acidosis with naloxone and noninvasive positive pressure ventilation.

A 74-year-old man was referred to our hospital due to deteriorating level of consciousness and desaturation. His Glasgow Coma Scale was 6, and his pupils were constricted but responded to light. Chest radiograph was negative for significant findings. Arterial blood gas evaluation on supplemental oxygen revealed severe acute on chronic respiratory acidosis: pH 7.15; PCO2, 133 mm Hg; PO2,64 mm Hg; and HCO3, 31 mmol/L. He regained full consciousness (Glasgow Coma Scale, 15) after receiving a 0.4 mg dose of naloxone, but because of persistent severe respiratory acidosis (pH 7.21; PCO2, 105 mm Hg), he was immediately commenced on noninvasive positive pressure ventilation (NIV) displaying a remarkable improvement in arterial blood gas values within the next few hours. However, in the days that followed, he remained dependent on NIV, and he was finally discharged on a home mechanical ventilation prescription. In cases of drug-induced respiratory depression, NIV should be regarded as an acceptable treatment, as it can provide ventilatory support without the increased risks associated with invasive mechanical ventilation.

[Clinical pathological study on 23 pulmonary embolism proved by autopsy].

To improve the early diagnosis of pulmonary embolism. The clinical and pathological data of 23 cases of autopsy-proved pulmonary embolism in Beijing hospital from 1951 to 1994 were reviewed. 23 patients: male 18, female 5, age ranged from 34 to 82 years. Misdiagnosis rate was 87%. The unexplained dyspnea, chest pain, sudden onset dyspnea and sudden death were the most frequent symptoms. Arterial blood gas data frequently demonstrated hypoxia and hypocapnia. The most important causes of an incorrect diagnosis could be the failure of suspecting pulmonary embolism, because of the variability of clinical manifestation and the presence of other concomitant diseases. All patients with otherwise severe unexplained dyspnea or chest pain have to be sent for perfusion lung scintigraphy, accordingly, underdetection of pulmonary embolism and mortality of pulmonary embolism could be reduced.

Blood

The term serum refers to plasma from which the clotting proteins have been removed. Most of the proteins remaining are albumin and immunoglobulins. pH values Blood pH is regulated to stay within the narrow range of 7.35 to 7.45, making it slightly basic. Blood that has a pH below 7.35 is too acidic, whereas blood pH above 7.45 is too basic. Blood pH, partial pressure of oxygen (pO2), partial pressure of carbon dioxide (pCO2), and bicarbonate (HCO3−) are carefully regulated by a number of homeostatic mechanisms, which exert their influence principally through the respiratory system and the urinary system to control the acid–base balance and respiration. An arterial blood gas test measures these. Plasma also circulates hormones transmitting their messages to various tissues. The list of normal reference ranges for various blood electrolytes is extensive. In non-mammalian vertebrates

[The diagnosis of pulmonary embolism: the role of noninvasive technics].

Today a large group of patients with pulmonary embolism is still undetected because this disease is not suspected. We evaluated the role of routine clinical procedures such as history, chest x-ray, electrocardiogram and blood gas analysis in the diagnosis of this disease. We studied 177 patients sent to our observation with suspicion of pulmonary embolism, which was later confirmed in 97 and excluded in 80. Prolonged immobilization, surgical procedures and deep vein thrombosis are the most frequent predisposing factors (P less than 0.05 or less) in patients with pulmonary embolism with respect to patients with unconfirmed suspicion of embolism. Among symptoms and signs, pleuritic chest pain, sudden onset of dyspnea, tachypnea, fever, enlarged jugular veins, enhanced pulmonary component of the second heart sound, pulmonary systolic murmur and basal hypophonesis were the most frequent signs (P less than 0.005 or less) in patients with embolism. Among radiographic signs "sausage" descending pulmonary artery, diaphragmatic elevation, pulmonary infarction, Westermark sign and azygos vein enlargement were more frequent (P less than 0.05 or less) in patients with embolism with respect to patients with unconfirmed suspicion of embolism. Among electrocardiographic signs, tachycardia, P-R segment displacement and negative T wave in V1-V2 were more frequent in patients with embolism with respect to patients with unconfirmed suspicion of embolism (P less than 0.05 or less). PO2, standard pO2 and pCO2 were significantly lower (P less than 0.001) in patients with embolism. After discriminant analysis of the whole data set most patients were correctly classified as embolic (90/97) and non-embolic (75/80).(ABSTRACT TRUNCATED AT 250 WORDS)

[Acute encephalopathy due to thiamine deficiency with hyperammonemia in a chronic hemodialysis patient: a case report].

Hemodialysis(HD) patients are at risk for thiamine deficiency because of low intake and accelerated loss of thiamine during HD. We report here an HD patient, an 82-year-old woman, who developed acute encephalopathy due to thiamine deficiency with hyperammonemia. She was admitted to Nishikawa Town Hospital due to pneumonia and was treated with ABPC/SBT for one week. While she was cured of pneumonia, she had a persistently poor appetite. On the twenty-fourth day after admission, HD with intradialytic parenteral nutrition(IDPN), which consisted of 10% glucose 500 ml, in order to correct her malnutrition, was started. She suddenly presented confusion, speech disturbance and ophthalmoplegia. HD with IDPN was stopped after two hours because of her symptoms. Laboratory studies disclosed plasma glucose of 186 mg/dl and serum ammonium of 155 micrograms/dl. Arterial blood gas analysis(inhaling 3 l/min O2) showed severe metabolic acidosis and respiratory acidosis (pH 7.138, pCO2 44.8 mmHg, pO2 108.9 mmHg, HCO3- 15.1 mmol/l). Her malnutrition, unexplained metabolic acidosis and neurological presentation raised the suspicion of acute encephalopathy due to thiamine deficiency. Fursultiamine 100 mg was administered intravenously. After two hours, metabolic acidosis disappeared (pH 7.437, pCO2 33.9 mmHg, pO2 161.0 mmHg, HCO3- 22.9 mmol/l), and she regained her clear consciousness and serum ammonium decreased at 16 micrograms/dl on the next morning. Serum lactate and thiamine level were shown later to be 57.5 mg/dl and 27 nmol/l, respectively. Her clinical course suggests that the glucose load including IDPN may have caused deterioration of the neurological disorder under the condition of thiamine deficiency. Furthermore, it is possible that a relationship exists between thiamine deficiency and hyperammonemia.

Tony Bland

Although Bland survived the initial crush, he had suffered severe brain damage and eventually became the disaster's 96th victim on 3 March 1993, aged 22, after being in a coma for nearly four years. He never regained consciousness and a legal ruling in November 1992 allowed doctors to withdraw his treatment at the request of his family, as there had been no sign of improvement in his condition and the doctors treating him advised that there was no reasonable possibility that he would ever emerge from his persistent vegetative state, and was unlikely to survive more than five years. Injuries and prognosis Bland suffered serious injuries in the crush at the Leppings Lane terrace. He suffered crushed ribs and two punctured lungs, causing an interruption in the supply of oxygen to his brain. As a result, he sustained catastrophic and irreversible damage to the higher centres of the brain, which had left him in a persistent vegetative state (PVS).

Pulmonary gas exchange and ventilation during hemodialysis.

Hemodialysis-induced hypoxemia has been explained by several mechanisms: pulmonary microembolization, decreased pulmonary diffusing capacity, fall in alveolar oxygen tension, hypoventilation and ventilation/perfusion abnormalities. The objective of this study was to analyze the factors influencing pulmonary ventilation and gas exchange of 20 patients with chronic renal failure during hemodialysis performed under the following conditions: Group 1 (9 patients) dialyzed against an acetate dialysate with a cuprophan membrane; Group 2 (7 patients) dialyzed against acetate bubbled with CO2 with a cuprophan membrane; Group 3 (4 patients) similar to Group 1, but using a polyacrylonitrile membrane. Arterial and venous blood samples were obtained from the respective lines during the predialysis period (zero), at 30, 60, 120 180 and 240 min of hemodialysis, and 60 min post dialysis (300 min) for the measurement of pH, PCO2, PO2, HCO-3 and total CO2. The minute expired volume (VE), expired fractions of O2 (FEO2) and CO2 (FECO2), O2 consumption (VO2), CO2 elimination through the lungs (VCO2) and dialyzer, respiratory exchange ratio (R), dead space to tidal volume ratio (VD/VT), alveolar ventilation (VA) and alveolar-arterial O2 difference (delta AaPO2) were measured and a leukocyte count was performed for each period of hemodialysis. The patients in Groups 1 and 3 showed a significant drop in ventilation and PaO2, a slight decrease in PAO2 and a significant increase in delta AaPO2. The patients in Groups 1 and 2 showed a significant leukopenia at 30 min of hemodialysis. The volume of CO2 eliminated across the dialyzer was very similar for the three groups of patients. Group 2 did not show any drop in ventilation or PaO2. For Group 2 venous line pH was very low and PCO2 was within the normal range, in contrast to the normal or high pH and low PCO2 shown by Groups 1 and 3. This study indicates that the drop in PaO2 was partially the consequence of a slight decrease in PAO2, but mainly due to the increase in delta AaPO2. Thus the most likely cause of the decrease in PaO2 was the VA/Q imbalance brought about by a drop in ventilation. The drop in ventilation was linked not only to the volume of CO2 eliminated across the dialyzer, but also to the amount of CO2 delivered to the lungs, and to the pH and PCO2 of the venous line.

[Analysis on treatment of extremely severe burn patients with severe inhalation injury in August 2nd Kunshan factory aluminum dust explosion accident].

<bObjective:</b To summarize the measures and experience in diagnosis and treatment of extremely severe burn patients with severe inhalation injury in dust explosion accident. <bMethods:</b The medical records of 13 patients with extremely severe burn complicated with severe inhalation injury in August 2nd Kunshan factory aluminum dust explosion accident who were treated at the First Affiliated Hospital of Soochow University (hereinafter referred to as our hospital) on August 2nd, 2014, were retrospectively analyzed. All the patients were transferred to our hospital 3-8 hours after injury under the condition of inhalation of pure oxygen. Twelve patients underwent tracheotomy within 5 hours after admission, while 1 patient underwent tracheotomy before admission. All the patients were in ventilator-assisted respiration, with synchronized intermittent mandatory ventilation combined with positive end expiratory pressure. All the patients underwent thorax or limbs escharotomy on the second day after admission, so as to reduce the restrictive ventilatory dysfunction caused by the contraction of thorax eschar and the terminal circulation disorder caused by the contraction of limbs eschar. All the patients underwent electronic bronchoscopy within 48 hours after admission, airway secretion were cleared and airway lavage were carried out under electronic bronchoscope according to the patients' condition, and the sputum, lavage solution, pathological tissue were collected for microbiological culture. All the patients underwent chest X-ray examination on the second day after admission and reexamination as required. Patients were all treated with a combination of broad-spectrum antibiotics early after admission to control lung and systemic infection. One patient was treated with extracorporeal membrane oxygenation for acute respiratory distress syndrome 1 week after admission. <bResults:</b One patient suffered from cardiopulmonary arrest during tracheotomy, which recovered autonomous respiration and cardiac impulse after cardiopulmonary resuscitation. Three patients showed decreased pulse oxygen saturation (SpO(2)) within 48 hours after injury, and the SpO(2) returned to normal after sputum aspiration, scab removal and lavage under electronic bronchoscope. During the course of disease, bacteria were cultured from wound exudate of 7 patients, bacteremia occurred in 10 patients, and sputum microbiological culture results of 13 patients were positive. Eight of the 13 patients in this group survived, and 5 died. One patient died 19 days after injury, and 4 patients died 33-46 days after injury. The main cause of death was multiple organ dysfunction syndrome induced by severe septic shock eventually. <bConclusions:</b For this batch of patients with extremely severe burn complicated with severe inhalation injury caused by dust explosion accident, the treatment and cure measures including early definite diagnosis and timely tracheotomy, the application of effective ventilation, the effective treatment of respiratory system complications, and rational use of antibiotics for the control of lung infection obtained quite good curative effect.

Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis.

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?

[Exercise tests in pneumopathy patients].

In this prospective work eleven pneumopathes patients were studied, ten of them with HAP, which were subjected to effort prove in endless band, in order to know the electrocardiographic alterations presented during the exercise. The VO2 máx was determined simultaneously in four patients. In the four, the value of this parameter was found under the normal value, which showed us a poor increase of the cardiac expense for the demands in the exercise. If the effort proves had not been practiced, this fact could not have been known. Related to the electrocardiographic alterations, cellular diastolic depolarization signs (cellular damage), product of the cellular damage, were found. The mechanics of this cellular damage, as well as the one of the poor increase of cardiac expense, are mentionned in the discussion.

[Dynamics of the acid-base balance of venous and arterial blood in clinically healthy calves].

Values of the acid base balance were examined in both venous and arterial blood of healthy calves (n = 6) of the Slovak Spotted breed aged, 3, 6, 8, 10, 12, 14, 18, and 24 weeks, respectively. Until week 4 of age the animals were fed milk only, until the age of 9 weeks a milk-roughage transition fodder and from week 10 on they were given classical herbage. Blood samples were taken from the V. jugularis and A. carotis communis or A. axillaris, respectively. The results achieved were corrected to a body temperature of 39 degrees C. During the examination period the following values were stated for both arterial and venous blood: actual acidity (pH) 7.391 +/- 0.014 and 7.362 +/- 0.013 logmolc, pCO2 6.35 +/- 0.15 and 7.35 +/- 0.11 kPa, HCO3-28.38 +/- 1.42 and 30.32 +/- 1.02 mmol. l(-1), ABE 3.57 +/- 1.44 and 4.34 +/- 1.09 mmol. l(-1); pO2 12.63 +/- 1.15 and 5.21 +/- 0.73 kPa, SAT 95.8 +/- 1.03 and 61.2 +/- 9.59%, respectively. A gradual increase in most indices of the acid base balance could be stated both in arterial and venous blood. The trends either revealed a parallel increase (HCO3-, pH) or they were more pronounced either in venous blood (SAT) or in arterial blood (ABE, pO2). Some trends were almost balanced (pCO2 and pO2 in venous blood and SAT and pCO2 in arterial blood). Thus pH, pO2 and SAT indices of the acid base balance were higher in arterial blood as compared to venous blood while pCO2, HCO3- and ABE values were higher in venous blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung Torsion -- History and Physical

No specific clinical signs or physical exam findings suggest lung torsion as the diagnosis. Nonspecific clinical signs include fever, chest pain, shortness of breath, and cough. [16] The most common symptom, however, are dyspnea, fever, and chest pain, respectively. [16] Most of these symptoms appear 4 to 14 days after a thoracic procedure, trauma, or any other triggering effect. Some patients were even asymptomatic and showed no clinical signs. Physical exam findings can reveal hypoxia, respiratory discomfort, and tachypnea. [13] [16] [21] [18] [1] Radiological imaging, however, is required to confirm the diagnosis of lung torsion. [22]

Carotid body

Stimulus The carotid body peripheral chemoreceptors are primarily sensitive to decreases in the partial pressure of oxygen (PO2). This is in contrast to the central chemoreceptors in the medulla oblongata that are primarily sensitive to changes in pH and PCO2 (a decrease in pH and an increase in PCO2). The carotid body chemoreceptors are also sensitive to pH and PCO2, but only secondarily. More specifically, the sensitivity of carotid body chemoreceptors to decreased PO2 is greater when pH is decreased and PCO2 is increased. Impulse rate for carotid bodies is particularly sensitive to changes in arterial PO2 in the range of 60 down to 30 mm Hg, a range in which hemoglobin saturation with oxygen decreases rapidly. The output of the carotid bodies is low at an oxygen partial pressure above about 100mmHg (13,3 kPa) (at normal physiological pH), but below 60mmHg the activity of the type I (glomus) cells increases rapidly due to a decrease in hemoglobin-oxygen saturation below 90%.

Clinical aspects of farmer's lung: airway reactivity, treatment and prognosis.

This study reviews the results of five clinical studies dealing with farmer's lung (FL). The total number of patients included was 107, with a mean age of 49 years. All patients were farmers with dairy cattle. The clinical symptoms, auscultatory findings, chest radiography, laboratory data, partial pressure of oxygen in arterial blood at rest (PaO2), dynamic spirometry (FVC and FEV1) and lung diffusing capacity of carbon monoxide (DLco) were recorded at the first visit to the hospital and one, three, six and twelve months later during the follow-up and every six months after that. Half of the patients with FL reported insidious onset of the disease, and 28% reported acute onset. Dyspnoea was reported by all patients, coughing was almost as common. A considerable proportion of the patients reported muscle and joint pains. Diffuse opacities were detected in the chest radiograms of 99 patients (93%): the more severe the radiological change, the more impaired the DLco value. A normal chest radiogram was seen in eight of the 107 patients at the first evaluation. Half of the patients showed a restrictive type of impairment of ventilatory function at the first evaluation. Lung diffusing capacity was less than 80% of the predicted value in 89% of the patients. Ninety-nine patients were initially challenged with histamine and twenty-two of them (22%) showed increased bronchial responsiveness. Bronchial hyper-reactivity was transient in most of the patients and might also fluctuate with exacerbation of FL symptoms. Specimens of the airway epithelium of FL patients were taken by rigid bronchoscope from five patients for electronmicroscope studies. Extensive bronchial damage to the airway epithelium associated with the presence of spore-like fungi was observed. Aspiration biopsy of the spleen was carried out on ten FL patients during their first visit to the hospital. Granuloma-like reactions were detected in the aspiration biopsy material of five FL patients. The granulomatous changes in the spleen had disappeared when the procedure was repeated on two patients at an asymptomatic stage of the disease. Ninety-three patients were included in a follow-up study with a mean follow-up period of 18.6 months. The patients with clinically less severe disease were observed without medication. It appeared that corticosteroid medication was usually started if the DLco value was less than 65% of the predicted value. Fourteen patients with a DLco value less than 65% were observed without medication and served as a control group for those on medication.(ABSTRACT TRUNCATED AT 400 WORDS)

Spontaneous pneumomediastinum following pneumonia in a 23-year-old male patient.

Spontaneous pneumomediastinum (SPM) is defined as the presence of interstitial air in the mediastinum without any apparent precipitating factor. We present a case of 23 year old male patient, who has been referred to our outpatient clinic with the complaints of sudden chest pain, dyspnea followed by pneumonia and was diagnosed as SPM. The patient was treated with ampicillin sulbactam (4 gr/day) and methylprednisolon (20 mg/day) for 4 days. and oral intake was stopped during treatment. Post treatment, it was observed that the crepitations were disappeared thoroughly and vesicular sounds were heard by oscultation. The control values of arterial blood gas was as following: pH:7,39 pO2:95 mmHg, pCO2:37 mmHg, SaO2: %97. In the 5th day his oral intake was started and he was discharged.


The closest answer is 1. If we are strict we would be talking about a pure motor lacunar infarction (with mild dysarthria). Since the other 3 options do not give us a clinical picture like the one in the statement. Both options 2 and 3 give us a much more florid and extensive clinical picture.

[HIDDEN] If we are strict we would be talking about a pure motor lacunar infarction (with mild dysarthria). Since the other 3 options do not give us a clinical picture like the one in the statement. Both options 2 and 3 give us [HIDDEN] extensive clinical picture.

In a 70-year-old man, hypertensive, with a right hemiplegia of sudden onset with mild dysarthria, without alterations in evocation or language comprehension, what type of stroke do you think is most likely to have suffered?

Left capsular lacunar lacunar infarction.

A cortico-subcortical left frontotemporal sylvian infarction.

[Aphasias for verbal and sign languages are due to lesions of nearly localised but not identical brain regions of the left hemisphere].

To study the characteristics of verbal and sign language aphasia in a patient fluent in both languages, who had had a recent left hemisphere stroke as well as to localise the site responsible for Spanish sign language aphasia. 56 years old male, with risk factors for stroke, who presented an episode of sudden onset aphasia and right hemiplegia that partially recovered in a few hours. The residual deficit of language was explored with a detailed protocol that included comprehension, denomination, oral and phonetic praxis, propositional and automatic spontaneous language, reading and writing tasks. The examination of verbal and sign language was video-recorded. The lesion was localised by magnetic resonance imaging 24 days after the stroke. The patient, whose infarction involved the superior temporal gyrus and sylvian operculum, presented similar abnormalities for comprehension of complex sentences, many phonemic paraphasias and no trouble to repeat single words. Oral language was not fluent, but sign language was quite fluent with a rich vocabulary, but with semantic paraphasias, agrammatism and without self-criticism for his own mistakes. The pattern of oral and sign language alterations is partially different, more for expressive than perceptive discourse, although both types of aphasias are caused by lesions of the left hemisphere. The regions responsible for these abnormalities of both symbolic languages are localised close to each other, but not in the same place.

Lacunar stroke

Signs and symptoms Each of the five classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (e.g., the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical signs (aphasia, visuospatial neglect, gaze deviation, and visual field defects) are always absent in lacunar strokes. The classic syndromes are as follows: Silent lacunar infarction

Neurology_Adams

As mentioned, in the ventral pons, the lacunar syndrome may be one of pure motor hemiplegia, mimicking that of internal capsular infarction except at times for relative sparing of the face and the presence of an ipsilateral paresis of conjugate gaze in some cases; or there is another highly characteristic lacunar syndrome of a combination of dysarthria and clumsiness of one hand. This “clumsy hand–dysarthria” stroke is usually located in the paramedian midpons or in the posterior portion of the internal capsule opposite the affected limb. Occasionally, a lacunar infarction of the pons, midbrain, internal capsule, or parietal white matter gives rise to a hemiparesis with ataxia on the same side as the weakness (Fisher, 1965a; Sage and Lepore). Some of the brainstem syndromes may blend with basilar branch syndromes.

Neurology_Adams

Lacunar strokes tend to evolve quickly but not typically as suddenly as an embolus, for example. These clinical aspects are discussed extensively in the earlier section “Lacunar TIA.” In broad terms, the essential feature of these deep strokes is the striking absence of cortical deficits; that is, seizures, aphasia or amnesia (except in limited circumstances of small thalamic infarction), agnosia, apraxia, dysgraphia, alexia, and a number of cognitive changes. Multiple deep strokes can result in a dementia of the type discussed in Chap. 20. Furthermore, because of the small size of the strokes, certain clinical syndromes that might be expected to result from deep lesions, such as hemianopia, also do not occur. Fisher, in several papers (1965a, 1967, 1979) and in an iconic review 1965b, delineated the most frequent symptomatic forms of lacunar stroke: 1. Pure motor hemiplegia 2. Pure sensory stroke 3. Clumsy hand–dysarthria 4. Ipsilateral hemiparesis–ataxia

Lacunar Stroke -- History and Physical

Clinical presentation depends on the area of brain involvement. Lacunar infarcts in the centrum semiovale may present without symptoms and can be found incidentally on brain imaging for some other cause. However, certain lacunar infarcts, like in the posterior limb of the internal capsule or the pons, can present with severe hemiplegia. Often, cortical findings, such as neglect, visual disturbances, aphasia, and behavioral changes, are absent in the clinical presentation of lacunar stroke as they occur in subcortical areas of the brain.

Lacunar Syndromes -- History and Physical

Sensorimotor Stroke : Patients present with weakness and numbness of the face, arm, and leg without cortical signs. Cortical function testing should distinguish between a frontoparietal lobe (MCA) stroke and a subcortical stroke (posterior thalamus and internal capsule). Dysarthria-Clumsy Hand Syndrome : This is a less common form of the lacunar syndrome. Patients present with facial weakness, dysarthria, dysphagia, and dysmetria or clumsiness of one upper extremity.

Neurology_Adams

It has been recognized that strokes caused by occlusion of small penetrating vessels of the brain—lacunes—have a propensity to be intermittent (“stuttering”) at their onset and occasionally to allow virtually complete restitution of function between discrete episodes. Whether this constitutes a “lacunar TIA” has been debated, but it seems to us that the more important problem is our inability to distinguish a transitory occlusion of a small vessel from that of a larger vessel. Donnan and colleagues (1993) speak of a “capsular warning syndrome,” which we have seen a number of times, consisting of escalating episodes of weakness in the face, arm, and leg and culminating in a capsular lacunar stroke. Nevertheless, the basic pattern of a small deep stroke remains identifiable in mild form; partial syndromes that simulate cortical TIA are less common. Lacunar stroke is discussed extensively further on.

Clinical study of 39 patients with atypical lacunar syndrome.

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.

Lacunar Stroke -- History and Physical

Pure motor hemiparesis involves the posterior limb of the internal capsule, corona radiata. This type presents with contralateral hemiparesis of the face, arm, and leg. Mild dysarthria may be present with the absence of sensory symptoms. These are the most common lacunar syndromes. They account for 45% of cases of lacunar strokes. Cortical signs like aphasia, cognitive deficit, or visual symptoms are always absent. Pure motor stroke can be a combination of weakness in the arm, leg, or face on one side or any of these parts alone.

Neurology_Adams

Many diseases and focal cerebral lesions mute or reduce the prosody of speech, the most dramatic examples being the hypophonic monotone of Parkinson disease and the effortful utterances of Broca’s aphasia. Largely through the work of Ross, it has become apparent that prosody is also greatly disordered in patients with strokes involving portions of the nondominant hemisphere that mirror the language areas of the left hemisphere. In these cases, there is impairment both of comprehension and of production of the emotional content of speech and its accompanying gestures. A prospective study of middle cerebral artery infarctions by Darby corroborated this view: aprosodia, as it has come to be called, was present only in those patients with lesions in the territory of the inferior division of the right middle cerebral artery. The deficit was most prominent soon after the stroke and was not found with lacunar lesions. In our patients, using bedside tests, we have had difficulty in

Lacunar stroke

Treatment and prognosis Typically, tissue plasminogen activator may be administered within 3 to 4.5 hours of stroke onset if the patient is without contraindications (i.e. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Anticoagulants such as heparin and warfarin have shown no benefit over aspirin with regards to five-year survival. Patients who suffer lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise.

[Case of ipsilateral monoparesis by lacunar infarction: a consideration on the pathological mechanism].

An 81-year-old man had sudden-onset dysarthria and weakness in the right leg, and was admitted to our hospital in July 2009. Neurological examination showed right leg monoparesis, sensory disturbance on the right limbs, dysarthria, and decreased deep tendon reflexes. Brain MRI revealed an acute lacunar infarction in the right corona radiata and an old lacunar infarction in the left centrum semiovale, which occurred 4 years before. MR tractography disclosed impaired motor fibers in the right corona radiata, and transcranial magnetic stimulation (TMS) suggested diminished innervation from the bilateral cerebral cortices to the right leg. These results collectively indicated that reorganization of the pyramidal fibers were responsible for the monoparesis ipsilateral to the lacunar infarction, although anomalous pyramidal fibers with ipsilateral innervation were responsible for ipsilateral hemiplegia a previous study.

Neurology_Adams

This rare and somewhat amusing condition defies classification but is worthy of comment because it may be mistaken for hysteria or psychosis. An accent that is distinctly foreign but vague in actual region of origin replaces the patient’s native speech pattern. The syndrome arises after a left-sided lesion, most often a stroke with a mild associated Broca aphasia. Although the accent may be interpreted by the listener as compatible with German, Spanish, French, Asian, or another nationality, authoritative analysis indicates that the alterations are not specific to any genuine language and are simply attributed by the listener to a known foreign accent. The syndrome is also encountered as a transient phenomenon during recovery from stroke. The relation to disorders of prosody, which is produced by lesions of the nondominant hemisphere, is unclear. LeCours and Lhermitte made an analysis of the disorder based on the obligate use of diphthongs in certain languages; these were not properly

Lipohyalinosis

Furthermore, "In the microscopic level of small arteries or arterioles, hypertension also generates specific vasculopathies such as lipohyalinosis and thus causing lacunar infarctions". Hypertensions and lacunar infarcts and lacunar stroke are related. This means hypertension is a start to a chain reaction. From lipohyalinosis to lacunar infarctions that may eventually lead to stroke, hypertension, uncontrolled, can cause a lot of damage to the brain. Lacunar infarcts Lacunar infarcts are a result of atherosclerosis (microthrombi) and lipohyalinosis. These affect the deep structures of the brain and may leave small (~5mm) cavity lesions. Small lacunar infarcts are "caused by various arterial disorders, the most frequent of which include microatheroma, lipohyalinosis, fibrinoid necrosis, and Charcot-Bouchard aneurysm".

Sign language in the brain

damage in Broca's area have problems producing signs. Those with damage in the Wernicke's area (left hemisphere) in the temporal lobe of the brain have problems comprehending signed languages. Early on, it was noted that Broca’s area was near the part of the motor cortex controlling the face and mouth. Likewise, Wernicke's area was near the auditory cortex. These motor and auditory areas are important in spoken language processing and production, but the connection to signed languages had yet to be uncovered. For this reason, the left hemisphere was described as the verbal hemisphere, with the right hemisphere deemed to be responsible for spatial tasks. This criteria and classification was used to denounce signed languages as not equal to spoken language until it was widely agreed upon that due to the similarities in cortical connectivity they are linguistically and cognitively equivalent. In the 1980s research on deaf patients with left hemisphere stroke were examined to explore

Global aphasia

subcortical regions. It is well known that a lesion to the cortex can cause aphasia. However, a study by Kumar et al. (1996) suggests that lesions to the subcortical regions of the cortex such as the thalamus, basal ganglia, internal capsule, and paraventricular white matter can also cause speech and language deficits. This is due to the fact that the subcortical regions are closely associated with the language centers in the brain. Kumar et al. state that while lesions to the subcortical regions could cause certain types of aphasia, a lesion to these regions would rarely cause global aphasia. In a study performed by Ferro (1992), it was found that five different brain lesion locations were linked to aphasia. These locations include: "fronto-temporo-parietal lesions", "anterior, suprasylvian, frontal lesions", "large subcortical infarcts", "posterior, suprasylvian, parietal infarcts", and "a double lesion composed of a frontal and a temporal infarct".

Neurology_Adams

Levine DN, Mohr JP: Language after bilateral cerebral infarctions: Role of the minor hemisphere in speech. Neurology 29:927, 1979. Lundgren K, Helm-Estabrooks N, Klein R: Stuttering following acquired brain damage: A review of the literature. J Neurolingustics 23:447, 2010. Martin N, Saffran EM: A computational account of deep dysphasia: Evidence from a single case study. Brain Lang 43:240, 1992. Milner B, Branch C, Rasmussen T: Evidence for bilateral speech representation in some non-right-handers. Trans Am Neurol Assoc 91:306, 1966. Mohr JP: The vascular basis of Wernicke aphasia. Trans Am Neurol Assoc 105:133, 1980. Mohr JP, Pessin MS, Finkelstein S, et al: Broca aphasia: Pathologic and clinical. Neurology 28:311, 1978. Naeser MA, Alexander MP, Helm-Estabrook N, et al: Aphasia with predominantly subcortical lesion sites. Arch Neurol 39:2, 1982. Ojemann G: Cortical organization of language. J Neurosci 11:2281, 1991.

Neuroanatomy, Internal Capsule -- Clinical Significance -- Ischemic Strokes Involving the Internal Capsule

Lacunar strokes primarily affect the deep structures of the brain, such as the putamen, caudate nucleus, thalamus, and internal capsule. Depending on the location of a lesion, the symptoms of lacunar strokes will require differentiation from cortical strokes. These deep strokes usually have an absence of cortical deficits such as seizures, aphasia, agnosia, and dysgraphia. Other cortical deficits include apraxia, alexia, and amnesia. The progression of symptoms of lacunar strokes are abrupt in onset and evolve within minutes. [20] In some cases, the symptoms may develop over several hours. Many variations of lacunar stroke syndromes exist. Classic lacunar stroke syndrome that arises from internal capsule lesions are pure motor strokes, ataxic hemiparesis, and clumsy hand-dysarthria. [21]

Lacunar stroke

Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as suffering from lacunar stroke syndrome (LACS). Much of the current knowledge of lacunar strokes comes from C. Miller Fisher's cadaver dissections of post-mortem stroke patients. He observed "lacunae" (empty spaces) in the deep brain structures after occlusion of 200–800 μm penetrating arteries and connected them with five classic syndromes. These syndromes are still noted today, though lacunar infarcts are diagnosed based on clinical judgment and radiologic imaging. Signs and symptoms

Neurology_Adams

Kurowski KM, Blumstein SE, Alexander M: The foreign accent syndrome: A reconsideration. Brain Lang 54:1, 1996. LeCours H, Lhermitte F: Aphasiology. Eastbourne, UK, Ballière-Tindall, 1989. LeCours H, Lhermitte F: The pure form of the phonetic disintegration syndrome (pure anarthria). Brain Lang 3:88, 1976. Leiner HC, Leiner SL, Dow RS: Cognitive and language functions of the human cerebellum. Trends Neurosci 16:444, 1993. Leischner A: The agraphias. In: Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology. Vol 4: Disorders of Speech, Perception and Symbolic Behavior. Amsterdam, North-Holland, 1969, pp 141–180. LeMay M, Culebras A: Human brain morphologic differences in the hemispheres demonstrable by carotid angiography. N Engl J Med 287:168, 1972. Levine DN, Mohr JP: Language after bilateral cerebral infarctions: Role of the minor hemisphere in speech. Neurology 29:927, 1979.

Lacunar stroke

A silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward symptoms, and is thus termed "silent." Because stroke is a clinical diagnosis (that is, it is defined by clinical symptoms), there is debate about whether SLI are considered to be strokes, even though the pathophysiology is presumably the same. Individuals who suffer a SLI are often completely unaware they have suffered a stroke. This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computed axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the

Selective associative phonagnosia after right anterior temporal stroke.

We report the case of a 48 year old men who developed a selective impairment in famous voice recognition after ischemic stroke in right subcortical structures (lenticular nucleus and head of the caudate) and right anterior temporal lobe. He underwent fibrinolytic treatment. During the following days he progressively recovered and was discharged without neurological focal sign. Patent foramen ovale was found. When he got back to his house he noticed that he was unable to recognize the voice of his favoured singers and needed to ask who was the singer to his relatives. Neuropsychological examination revealed a selective impairment in famous voice recognition in the absence of alteration of voice perception, face perception and famous face recognition. All other neuropsychological domains were spared. In particular language, memory and executive functions were intact. Neuroimaging carried out by means of PET and MRI revealed two small ischemic lesions in the right subcortical region, involving lenticular and caudate nuclei and in the right temporal pole. To our knowledge, this is the first case described in literature of a patient showing a selective associative phonagnosia after right anterior temporal stroke. The present case helps to clarify the brain circuits underlying famous voice recognition and adds evidence in favour of a right hemisphere involvement in processing knowledge of familiar voices. These findings are discussed in relation to current models of brain organization of person-specific and general semantic knowledge.

Cerebral small vessel disease in pseudoxanthoma elasticum: three cases.

Cerebral small vessel disease is rarely described in association with pseudoxanthoma elasticum (PXE), a hereditary connective tissue disorder with skin, eye and vascular manifestations. This autosomally inherited elastic tissue disease has been attributed to mutations in the ABCC6 gene located on chromosome 16p13.1. Different stroke mechanisms are suggested in PXE patients, arterial hypertension and accelerated atherosclerosis being the leading ones. Case 1: A 49-year-old man with history of mild hypertension presented with recurrent transient ischemic attacks. At the age of 42, evaluation for progressive visual loss and skin changes led to diagnosis of PXE. Brain magnetic resonance imaging (MRI) disclosed multiple lacunar infarctions and confluent periventricular white matter lesions (WML). Case 2: A 71-year-old woman with history of mild hypertension suffered right-sided stroke. Diagnosis of PXE was made at the age of 48 due to severe visual loss and skin changes. Brain MRI revealed multiple lacunar infarctions and subcortical ischemic leukoencephalopathy. Case 3: A 47-year-old woman with prominent skin changes and bilateral amblyopia developed right-sided weakness. Skin biopsy confirmed PXE. Several lacunar infarcts in deep white matter and pons were revealed on MRI. We present three patients with clinical and histopathological features of PXE who presented with multiple lacunar strokes, two with extensive confluent WML. These cases illustrate that PXE is a rare but significant risk factor for small vessel disease and stroke in patients of all age groups. Occlusive small vessel disease and subsequent lacunar infarcts and WML represent important PXE manifestations.

[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset].

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.

Neurology_Adams

Motor speech disorders, both severe Broca aphasia and the more restricted and transient types, are most often a result of vascular lesions. Embolic stroke in the territory of the upper (rolandic, superior) division of the middle cerebral artery is the most frequent type and results in an abrupt onset of aphasia. Small strokes may give way to rapid improvement (hours to days); contrariwise, infarctions that extend beyond the central Broca region at times produce a more severe clinical syndrome than might be anticipated from the size of the lesion. It is these latter strokes, especially if the underlying frontal white matter is damaged, that tend to cause lasting speech difficulty. Because of the territory that is supplied by the superior branch of the middle cerebral artery, strokes that cause Broca aphasia are usually associated with right-sided brachiofacial paresis (face, proximal arm, and hand) as described earlier, and sometimes with a left-sided manual-brachial apraxia

First_Aid_Step1

Hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels G ), followed by thalamus, pons, and cerebellum H . Effects of strokes Anterior circulation Middle cerebral artery Motor and sensory cortices A —upper limb and face. Temporal lobe (Wernicke area); frontal lobe (Broca area). Contralateral paralysis and sensory loss—face and upper limb. Aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion affects nondominant (usually right) hemisphere. Wernicke aphasia is associated with right superior quadrant visual field defect due to temporal lobe involvement. Lenticulo-striate artery Striatum, internal capsule. Contralateral paralysis. Absence of cortical signs (eg, neglect, aphasia, visual field loss). Pure motor stroke. Common location of lacunar infarcts B , due to hyaline arteriosclerosis (lipohyalinosis) 2° to unmanaged hypertension. Posterior circulation

A 15-year-old boy with central nervous system vasculopathy presenting with dysarthria-clumsy hand syndrome.

Dysarthria-clumsy hand stroke syndrome has been described frequently in adults but not in children. We report a 15-year-old right-handed boy with sudden onset of dysarthria, dysphagia, right facial weakness, and mild right-hand clumsiness. Computed tomographic scan and magnetic resonance imaging demonstrated infarction in the genu and posterior limb of the left internal capsule. Magnetic resonance angiography and conventional angiography demonstrated stenosis of the supraclinoid portion of the left internal carotid artery and the origin of the left ophthalmic artery. Lacunar infarction in an older adult is not the only mechanism leading to dysarthria-clumsy hand syndrome.

[Cerebrovascular disorder and the language areas].

Recent progress of imaging techniques has achieved precise descriptions of aphasic syndromes associated with cerebrovascular disorders. Infarction of the left anterior cerebral artery brings about transcortical motor aphasia. Occlusion of each branches of the left middle cerebral artery produces characteristic language symptoms. Recently, cases with infarction of the areas of prefrontal and precentral arteries were reported to manifest fluent aphasia indistinguishable from the classical transcortical sensory aphasia. Rare cases with lesions restricted to the Broca's area (territory of the precentral artery) produces aphasia with normal fluency, word finding difficulty and deficit in sentence comprehension. Classical non-fluent Broca's aphasia is caused by infarctions which at least involves the areas of precentral and central arteries. Aphemia or pure word dumbness results from damages which involves territory of the central artery. Conduction aphasia is most often associated with lesions of the posterior parietal artery territory. As in the case of Broca's aphasia, Wernicke's aphasia is a composite of conduction aphasia, pure word deafness, transcortical sensory aphasia, and alexia with agraphia. The lesion of Wernicke's aphasia naturally involves the areas of all of these aphasic symptoms. Transcortical sensory aphasia is associated with lesions in the posteroinferior temporal region, and is often associated with watershed infarctions of the middle and posterior cerebral arteries. Aphasia which results from putaminal hemorrhage has ambiguous manifestation, and is difficult to be classified into Wernicke-Lichtheim's model. Assessment of its fluency is notoriously difficult. Thalamic aphasia is similar to either anomic aphasia or transcortical sensory aphasia. It was pointed out that classical aphasic syndromes are still valid as cerebral arterial occlusion syndromes, but are insufficient for the purpose of more precise anatomo-clinical correlation.

[Multiple intracerebral microhemorrhages associated with primary aldosteronism: a case report].

We have observed dot-like low intensity spots (a dot-like hemosiderin spot: dotHS) on T2*-weighted (T2*-w) MRI, subsequently diagnosed histologically as previous microbleeds associated with lipohyalinosis, amyloid angiopathy and cerebral small vessel disease (SVD) including an intracerebral hematoma (ICH) and a lacunar infarction. According to the literature, primary aldosteronism (PA), characterized by hypertension, is related to SVD. A 49-year-old female with a long history of untreated hypertension secondary to PA was admitted to our hospital for medical examinations on July 18th, 2000. She had the stepwise development of dementia, dysarthria and gait disturbance (right hemiparesis). CT and MRI demonstrated multiple lacunar infarctions. She was readmitted to our hospital on Jan 23rd, 2002. A neurological examination revealed right hemiparesis, dysarthria and consciousness disturbance. CT on admission demonstrated ICH in the left midbrain. Six days after the hemorrhage, T2*-w MRI showed thirty-two dotHSs in the basal ganglias and the cortical-subcortical regions. The incidence of ICH in patients with hypertension secondary to PA is reported to be higher than in patients with essential hypertension. Multiple dotHS may be associated with ICH, lacunar infarction, and severe microangiopathy related to hypertension secondary to PA.

Hemisphere stroke: impact on the semantic lexical aspects of language.

To investigate if right hemisphere stroke is associated with decreased lexical-semantic ability. We compared subjects with right hemisphere brain damage after stroke with healthy controls using the validated version of the Montreal Evaluation of Communication to assess lexical-semantic domains of language. Sixteen patients and thirty-two controls were included. The post-stroke group with right hemispheric brain lesions showed considerable limitations in metaphor interpretation, fluency, and semantic judgment. Individuals with right hemisphere damage after stroke may present with language changes in the lexical-semantic aspects.

InternalMed_Harrison

Occlusion of a lenticulostriate vessel produces small-vessel (lacunar) stroke within the internal capsule (Fig. 4466). This produces pure motor stroke or sensory-motor stroke contralateral to the lesion. Ischemia within the genu of the internal capsule causes primarily facial weakness followed by arm and then leg weakness as the ischemia moves posterior within the capsule. Alternatively, the contralateral hand may become ataxic, and dysarthria will be prominent (clumsy hand, dysarthria lacunar syndrome). Lacunar infarction affecting the globus pallidus and putamen often has few clinical signs, but parkinsonism and hemiballismus have been reported.

Aphasia -- Pathophysiology

Aphasia is caused by lesions to the language areas of the brain, which are typically located in the dominant hemisphere. For the majority of the population, the dominant hemisphere is on the left side. [8] These areas are Wernicke area, Broca area, and arcuate fasciculus. The most common cause of aphasia is due to CVA. CVA occurs when the blood supply to a certain part of the brain is greatly diminished or stopped due to an ischemic event (i.e., embolism or thrombosis) or from a hemorrhagic event (i.e., intracerebral hemorrhage, subarachnoid hemorrhage). In some cases, aphasia can be caused by damage to subcortical structures deep within the left hemisphere, including the internal and external capsules, the thalamus, and the caudate nucleus. [9]