Intra-arterial therapy (IAT) has been used for three decades to promote recanalisation after stroke. Whereas results of the Prolyse in Acute Cerebral Thromboembolism-II trial (PROACT-II) showed significant improvement in clinical outcome with intraarterial fibrinolysis, the stroke specialty received some disturbing news in 2013. Results of the Interventional Management of Stroke-III (IMS-III), SYNTHESIS, and Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE) studies failed to show an increased benefit for IAT compared with intravenous alteplase (t-PA) or as an adjunctive approach to intravenous alteplase. [reference: Stroke roundup 2013. Lancet neurology, 2014]
The above description is for all IAT, not only for IAT of BA occlusion.
Although we continue to achieve high reperfusion rates with IAT, these successful radiographical outcomes do not always translate to good clinical outcomes. This gap raises the important issue of patient selection for IAT.
My comment: clinical outcome is the most important. Therefore, the important thing is whether and when the thrombolytic therapy should be done. As to the way of thrombolysis, IAT or IVT, I prefer IVT. Recognition of mode of onset is one of the important factors in making decision of intervention to treat BAO.
For those patients with high risk, prolonged low dose IVT may be a new treatment. This deserves further observation. [As to the issue about “Prolonged Low-Dose Thrombolysis in Posterior Circulation Stroke”, reference is Neurocrit Care. 2013 Nov 19. (Epub ahead of print)].
2014年1月3日 星期五
2013年11月4日 星期一
側記 Brodmann
Brodmann’s map是由德國內科醫師Krobinian Brodmann在1903至1908年間提出，有52區。
常謂塞翁失馬，焉知非福，在Brodmann身上，又是一例。Brodmann在他通過考試之後，原本是想從事臨床工作，然而卻不幸染上白喉，於是只得找一個比較輕鬆點的工作。所以他到Oskar Vogt的研究室，當一名研究助理；那時候是1896年5月，是他一生中的關鍵時刻：Vogt 當時正在籌建的Institute of Brain Research，十分吸引Brodmann，使得Brodmann再短暫追隨Vogt之後，又去Leipzig學pathology。在那裡，他拿到了醫學博士學位；然後，他再到Frankfurt 的University Psychiatric Clinic，接受Otto Binswanger的指導。從1900至1901年間，他在Frankfurt共待了18個月，當時在Frankfurt有一群既傑出又有衝勁的神經解剖學家，Brodmann身處其間，似飲曹溪一滴水，受益匪淺。Brodmann也是在那時候，遇上了Alois Alzheimer。Alzheimer 從1882年到1902年一直待在Frankfurt，當時他和Nissl密切合作，仔細地觀察大腦皮質之組織病理(histopathology)。
在1901年的秋天，Brodmann又回到Oskar Vogt在Berlin新成立的研究室。在那裡，他又遇到了Max Bielschowsky這位很會染神經纖維的大師。從1901年到1910年，就在Vogt的實驗室裡，Bielschowsy與Brodmann分工合作：Bielschowsy所負責的fibrilloarchitectonics及myelinoarchitectonics (based on the onset of myelination in different brain regions) 是Oskar Vogt的最大興趣，而Brodmann則負責cytoarchitectonics的研究。自1903年至1908年陸續發表很多papers來描述fine structure of cerebral cortex in a number of mammals (特別是primates)，而在1909年發表鉅著Vergleichende Lokalisationslehre der Grosshirnrinde [Localization in the cerebral hemisphere: a comprehensive study]。雖然Brodmann並不是史上唯一研究cytoarchitectonics的人，然而他提出的map，特別是他賦予每個區域的編號，卻是永垂青史。
精誠所至，金石為開。能做出這樣的事業，必有相當堅定的信念在他心裡。Brodmann想要為人所不敢為。當時的神經學者，腦中有個古怪的念頭，認為人的腦子既然負責一些心理及行為上的功能，那麼在腦子裡就應存有〝memory〞cell或〝psychi〞cell。但是Brodmann並不這麼認為。他認為這些心理或行為上的表現，並非僅憑單一細胞，而得靠一群細胞(cell grouping)才能達成這些表現。所以在他的腦子哩，有這麼兩種假說：
第一、物以類聚：意即，相似的細胞會聚在一起；
第二、細胞結構簡單者，其功能就簡單，不會複雜。
Brodmann服膺Bernhard Gudden所言，認為若想要研究function localization，必先研究出anatomy的具象事實，藉此才能衍生physiology的抽象觀念；若是先有physiology的理論，缺乏anatomy基礎，那麼一切可能流於虛妄空談。且不論他所想的兩種假說是否正確，不過以上的信念迄今仍被傳頌。
常謂塞翁失馬，焉知非福，在Brodmann身上，又是一例。Brodmann在他通過考試之後，原本是想從事臨床工作，然而卻不幸染上白喉，於是只得找一個比較輕鬆點的工作。所以他到Oskar Vogt的研究室，當一名研究助理；那時候是1896年5月，是他一生中的關鍵時刻：Vogt 當時正在籌建的Institute of Brain Research，十分吸引Brodmann，使得Brodmann再短暫追隨Vogt之後，又去Leipzig學pathology。在那裡，他拿到了醫學博士學位；然後，他再到Frankfurt 的University Psychiatric Clinic，接受Otto Binswanger的指導。從1900至1901年間，他在Frankfurt共待了18個月，當時在Frankfurt有一群既傑出又有衝勁的神經解剖學家，Brodmann身處其間，似飲曹溪一滴水，受益匪淺。Brodmann也是在那時候，遇上了Alois Alzheimer。Alzheimer 從1882年到1902年一直待在Frankfurt，當時他和Nissl密切合作，仔細地觀察大腦皮質之組織病理(histopathology)。
在1901年的秋天，Brodmann又回到Oskar Vogt在Berlin新成立的研究室。在那裡，他又遇到了Max Bielschowsky這位很會染神經纖維的大師。從1901年到1910年，就在Vogt的實驗室裡，Bielschowsy與Brodmann分工合作：Bielschowsy所負責的fibrilloarchitectonics及myelinoarchitectonics (based on the onset of myelination in different brain regions) 是Oskar Vogt的最大興趣，而Brodmann則負責cytoarchitectonics的研究。自1903年至1908年陸續發表很多papers來描述fine structure of cerebral cortex in a number of mammals (特別是primates)，而在1909年發表鉅著Vergleichende Lokalisationslehre der Grosshirnrinde [Localization in the cerebral hemisphere: a comprehensive study]。雖然Brodmann並不是史上唯一研究cytoarchitectonics的人，然而他提出的map，特別是他賦予每個區域的編號，卻是永垂青史。
精誠所至，金石為開。能做出這樣的事業，必有相當堅定的信念在他心裡。Brodmann想要為人所不敢為。當時的神經學者，腦中有個古怪的念頭，認為人的腦子既然負責一些心理及行為上的功能，那麼在腦子裡就應存有〝memory〞cell或〝psychi〞cell。但是Brodmann並不這麼認為。他認為這些心理或行為上的表現，並非僅憑單一細胞，而得靠一群細胞(cell grouping)才能達成這些表現。所以在他的腦子哩，有這麼兩種假說：
第一、物以類聚：意即，相似的細胞會聚在一起；
第二、細胞結構簡單者，其功能就簡單，不會複雜。
Brodmann服膺Bernhard Gudden所言，認為若想要研究function localization，必先研究出anatomy的具象事實，藉此才能衍生physiology的抽象觀念；若是先有physiology的理論，缺乏anatomy基礎，那麼一切可能流於虛妄空談。且不論他所想的兩種假說是否正確，不過以上的信念迄今仍被傳頌。
2013年5月11日 星期六
Buerger’s disease and cigarette filter
Adapted from Wikipedia
Buerger's disease was first reported by Felix von Winiwarter in 1879 in Austria. It wasn't until 1908 that the disease was given its first accurate pathological description, by Leo Buerger at Mount Sinai Hospital in New York City. Buerger called it "presenile spontaneous gangrene" after studying amputations in 11 patients.
It is strongly associated with use of tobacco products, primarily from smoking.
As to the structure of cigarette at that time, tobacco was simply wrapped by a piece of paper.
In 1925, inventor Boris Aivaz patented the process of making a cigarette filter from crepe paper. Aivaz produced the first cigarette filter from 1927, but uptake was low due to a lack of the machinery required to produce cigarettes with the filtered tip.
From 1935, a British company began to develop a machine that made cigarettes incorporating the tipped filter. Since filtered cigarettes were considered "safer", by the 1960s, they dominated the market.
Buerger's disease was first reported by Felix von Winiwarter in 1879 in Austria. It wasn't until 1908 that the disease was given its first accurate pathological description, by Leo Buerger at Mount Sinai Hospital in New York City. Buerger called it "presenile spontaneous gangrene" after studying amputations in 11 patients.
It is strongly associated with use of tobacco products, primarily from smoking.
As to the structure of cigarette at that time, tobacco was simply wrapped by a piece of paper.
In 1925, inventor Boris Aivaz patented the process of making a cigarette filter from crepe paper. Aivaz produced the first cigarette filter from 1927, but uptake was low due to a lack of the machinery required to produce cigarettes with the filtered tip.
From 1935, a British company began to develop a machine that made cigarettes incorporating the tipped filter. Since filtered cigarettes were considered "safer", by the 1960s, they dominated the market.
2013年2月16日 星期六
Reticular Reflex Myoclonus
The following sections about reticular reflex myoclonus was excerpted from Eplilesy textbook on 2013/02/16
Reticular reflex myoclonus originates in a hyperexcitable caudal brainstem reticular formation, giving rise to a widespread pattern of muscle activation with proximal and flexor predominance, spontaneous or induced by various stimuli. The impulses may travel up the brainstem. Reticular reflex myoclonus may be present simultaneously with cortical myoclonus.
Reticular reflex myoclonus is not time-locked to EEG discharges, and the sensory evoked potentials are not enhanced. Myoclonus is triggered by stimuli, but the temporal relationship is variable between the stimuli and the myoclonus, whereas it is constant in patients with cortical reflex myoclonus. The EMG discharges start in the areas of lower cranial nerves (sternocleidomastoid muscle, trapezius muscle). They go up to the facial muscles, down to the upper limbs, then to lower limbs. Therefore, it was speculated that the stimuli excited the reticular formation and that abnormal electrical activity then spread from it to the upper brainstem and the spinal cord.
Reticular reflex myoclonus originates in a hyperexcitable caudal brainstem reticular formation, giving rise to a widespread pattern of muscle activation with proximal and flexor predominance, spontaneous or induced by various stimuli. The impulses may travel up the brainstem. Reticular reflex myoclonus may be present simultaneously with cortical myoclonus.
Reticular reflex myoclonus is not time-locked to EEG discharges, and the sensory evoked potentials are not enhanced. Myoclonus is triggered by stimuli, but the temporal relationship is variable between the stimuli and the myoclonus, whereas it is constant in patients with cortical reflex myoclonus. The EMG discharges start in the areas of lower cranial nerves (sternocleidomastoid muscle, trapezius muscle). They go up to the facial muscles, down to the upper limbs, then to lower limbs. Therefore, it was speculated that the stimuli excited the reticular formation and that abnormal electrical activity then spread from it to the upper brainstem and the spinal cord.
Thalamocortical myoclonus
The following sections about thalamocortical myoclonus was excerpted from Eplilesy textbook on 2013/02/16
Thalamocortical myoclonus or idiopathic generalized epileptic myoclonus represents the common type of myoclonus in various epileptic syndromes. Myoclonia are often spontaneous, predominantly arrhythmic and axial with varying severity, and associated chronologically with an EEG pattern of diffuse polyspikes or (poly) spike-and-wave discharges. A hyperexcitable cortex is thought to be driven diffusely and synchronously by ascending subcortical inputs that trigger the paroxysmal events. As a consequence, muscles from both sides are activated, and muscles innervated by the cranial nerves are involved through a rostrocaudal manner.
Electrophysiologically, SEP usually does not show giant SEP, and C-reflex may be recorded at rest. A negative peak of the generalized spike (30–100 msec duration) precedes the jerk (<100 msec duration) by 20 to 75 msec. The latency of the spike is relatively longer, and the temporal relationship is looser than in that of cortical myoclonus. The underlying mechanism of the thalamocortical myoclonus is still uncertain. The myoclonus of benign myoclonic epilepsy of infancy, myoclonic-astatic epilepsy, and JME belongs to this category.
Myoclonus observed in patients with Dravet syndrome is not straightforward: Patients may exhibit massive myoclonus combined with a generalized spike-wave (rarely in infancy, mostly in childhood), and erratic myoclonus, particularly during episodes of myoclonic status, in which the patient is drowsy with diffuse slow wave activity and few spikes. The generator remains unidentified.
Thalamocortical myoclonus or idiopathic generalized epileptic myoclonus represents the common type of myoclonus in various epileptic syndromes. Myoclonia are often spontaneous, predominantly arrhythmic and axial with varying severity, and associated chronologically with an EEG pattern of diffuse polyspikes or (poly) spike-and-wave discharges. A hyperexcitable cortex is thought to be driven diffusely and synchronously by ascending subcortical inputs that trigger the paroxysmal events. As a consequence, muscles from both sides are activated, and muscles innervated by the cranial nerves are involved through a rostrocaudal manner.
Electrophysiologically, SEP usually does not show giant SEP, and C-reflex may be recorded at rest. A negative peak of the generalized spike (30–100 msec duration) precedes the jerk (<100 msec duration) by 20 to 75 msec. The latency of the spike is relatively longer, and the temporal relationship is looser than in that of cortical myoclonus. The underlying mechanism of the thalamocortical myoclonus is still uncertain. The myoclonus of benign myoclonic epilepsy of infancy, myoclonic-astatic epilepsy, and JME belongs to this category.
Myoclonus observed in patients with Dravet syndrome is not straightforward: Patients may exhibit massive myoclonus combined with a generalized spike-wave (rarely in infancy, mostly in childhood), and erratic myoclonus, particularly during episodes of myoclonic status, in which the patient is drowsy with diffuse slow wave activity and few spikes. The generator remains unidentified.
Cortical myoclonus
The following sections about cortical myoclonus was excerpted from Eplilesy textbook on 2013/02/16
Cortical myoclonus reflects impulses that originate in the sensorimotor cortex and travel down the brainstem. Cortical myoclonus is typically seen in progressive myoclonus epilepsy. Muscles involved tend to be distal more than proximal and flexor more than extensor, and to involve more the face and upper extremities than the rest of the body. Cortical myoclonus is more commonly encountered in a multifocal form, presenting with multifocal spike discharges. If myoclonus is triggered by stimuli, the term cortical reflex myoclonus is used. If myoclonus occurs periodically, the term epilepsia partialis continua is used. The neurons in the sensorimotor cortex may be primarily hyperexcitable, or may be driven by abnormal inputs from the neurons of other brain parts. Therefore, cortical myoclonus occasionally is called fragmented epileptic convulsion.
In patients with cortical reflex myoclonus, the cortical components of median-nerve SEP showed abnormally large amplitude. Usually, the initial peaks (N20/P22) are not large, and the following components become higher. This giant SEP is thought to indicate hyperexcitability of the sensorimotor cortex. Abnormally large evoked potentials were also reported by photic stimulation.
When the peripheral nerve is stimulated, the stimulus goes up the spino-thalamo-cortical tract and, after excitation of the pyramidal neuron, it goes down the cortico-spinal tract, resulting in muscle contraction (long-loop reflex). In normal subjects, long-loop reflex can be recorded only when subjects maintain muscle contractions. In patients with cortical reflex myoclonus, however, this reflex can be recorded even while resting (C-reflex). The latency of C-reflex for median nerve stimulation is about 40 to 45 msec, which is almost double of the latency of N20 to the median nerve stimulation. When the C-reflex is recorded from the contralateral limbs to the stimuli, the latency delay is about 10 msec to the ipsilateral limbs, which corresponds to the traveling time of the transcallosal pathway. This stimulation-locked muscle contraction is believed to share the same underlying mechanism with cortical reflex myoclonus.
Some EEG correlates are time-locked to cortical myoclonus. However, because of the relatively smaller amplitude of the EEG spikes in comparison with the background activities, the physiologic correlates of myoclonus can only be detected by using jerk-locked (EEG or magnetoencephalograhic [MEG]) averaging (JLA of jerk-locked magentic field [JLF]) or coherence analysis method. In JLA, EEGs are averaged with respect to the EMG onset, to reduce the non–time locked background EEG activities. Positive peak of the EEG spikes is 15 to 20 msec prior to the myoclonus for the upper limbs, and 25 to 40 msec for the lower limbs. Spikes are located around the contralateral primary motor cortex.
As such, cortical reflex myoclonus is caused by hyperexcitability of the primary sensorimotor cortex. However, because giant SEPs are not always present in patients with cortical reflex myoclonus (as in dentatorubral-pallidoluysian atrophy [DRPLA]), some other pathophysiologic mechanisms may exist.
In Lennox-Gastaut syndrome (LGS), myoclonus is rare and disclosed only in those cases with a cortical lesion affecting the rolandic area; thus, myoclonus appears to be produced by a secondary generalization of focal cortical myoclonus. They also present with arrhythmic, distal small focal jerks, leading to the individual tiny finger movements unaccompanied by premyoclonic potentials on JLA that Wilkins et al. proposed to call minipolymyoclonus. Brown et al. indicated that the major role of facilitation of inter- and intra-hemispheric spread of cortical myoclonic activity is through trans-callosal or intrahemispheric corticocortical pathways in producing generalized or bilateral myoclonus. Therefore, bilateral jerks may not be synchronous in patients with cortical myoclonus.
Cortical myoclonus reflects impulses that originate in the sensorimotor cortex and travel down the brainstem. Cortical myoclonus is typically seen in progressive myoclonus epilepsy. Muscles involved tend to be distal more than proximal and flexor more than extensor, and to involve more the face and upper extremities than the rest of the body. Cortical myoclonus is more commonly encountered in a multifocal form, presenting with multifocal spike discharges. If myoclonus is triggered by stimuli, the term cortical reflex myoclonus is used. If myoclonus occurs periodically, the term epilepsia partialis continua is used. The neurons in the sensorimotor cortex may be primarily hyperexcitable, or may be driven by abnormal inputs from the neurons of other brain parts. Therefore, cortical myoclonus occasionally is called fragmented epileptic convulsion.
In patients with cortical reflex myoclonus, the cortical components of median-nerve SEP showed abnormally large amplitude. Usually, the initial peaks (N20/P22) are not large, and the following components become higher. This giant SEP is thought to indicate hyperexcitability of the sensorimotor cortex. Abnormally large evoked potentials were also reported by photic stimulation.
When the peripheral nerve is stimulated, the stimulus goes up the spino-thalamo-cortical tract and, after excitation of the pyramidal neuron, it goes down the cortico-spinal tract, resulting in muscle contraction (long-loop reflex). In normal subjects, long-loop reflex can be recorded only when subjects maintain muscle contractions. In patients with cortical reflex myoclonus, however, this reflex can be recorded even while resting (C-reflex). The latency of C-reflex for median nerve stimulation is about 40 to 45 msec, which is almost double of the latency of N20 to the median nerve stimulation. When the C-reflex is recorded from the contralateral limbs to the stimuli, the latency delay is about 10 msec to the ipsilateral limbs, which corresponds to the traveling time of the transcallosal pathway. This stimulation-locked muscle contraction is believed to share the same underlying mechanism with cortical reflex myoclonus.
Some EEG correlates are time-locked to cortical myoclonus. However, because of the relatively smaller amplitude of the EEG spikes in comparison with the background activities, the physiologic correlates of myoclonus can only be detected by using jerk-locked (EEG or magnetoencephalograhic [MEG]) averaging (JLA of jerk-locked magentic field [JLF]) or coherence analysis method. In JLA, EEGs are averaged with respect to the EMG onset, to reduce the non–time locked background EEG activities. Positive peak of the EEG spikes is 15 to 20 msec prior to the myoclonus for the upper limbs, and 25 to 40 msec for the lower limbs. Spikes are located around the contralateral primary motor cortex.
As such, cortical reflex myoclonus is caused by hyperexcitability of the primary sensorimotor cortex. However, because giant SEPs are not always present in patients with cortical reflex myoclonus (as in dentatorubral-pallidoluysian atrophy [DRPLA]), some other pathophysiologic mechanisms may exist.
In Lennox-Gastaut syndrome (LGS), myoclonus is rare and disclosed only in those cases with a cortical lesion affecting the rolandic area; thus, myoclonus appears to be produced by a secondary generalization of focal cortical myoclonus. They also present with arrhythmic, distal small focal jerks, leading to the individual tiny finger movements unaccompanied by premyoclonic potentials on JLA that Wilkins et al. proposed to call minipolymyoclonus. Brown et al. indicated that the major role of facilitation of inter- and intra-hemispheric spread of cortical myoclonic activity is through trans-callosal or intrahemispheric corticocortical pathways in producing generalized or bilateral myoclonus. Therefore, bilateral jerks may not be synchronous in patients with cortical myoclonus.
Stereotypies
The following paragraph was taken from textbook "Neurology and clinical neuroscience" on 2013/02/05:
Stereotypies are repetitive, rhythmical, and invariant motor behaviors, without an apparent purpose or function, that can vary from simple motor behaviors such as rocking or hand waving to extraordinarily complex acts and rituals. They are one of the defining features of autism and are common in patients with mental retardation. Stereotypies are seen in adults with lesions or disorders affecting the frontostriatal circuit running between the dorsolateral frontal cortex and the head of the caudate nucleus. Frontotemporal dementias commonly manifest with stereotypic behaviors resulting from degeneration of the dorsolateral prefrontal cortex. Stimulant medications can produce complex stereotypies through a dopaminergic effect on the basal ganglia. Other repetitive motor behaviors such as compulsive behaviors and tics are seen in patients with Gilles de la Tourette syndrome and obsessive-compulsive disorder, both of which are considered to be associated with basal ganglia pathology. Of importance is that stereotypies, compulsions, complex tics, mannerisms (unusual or pathological styles of performing goal-directed activities, such as a bizarre gait and unusual ways of greeting people), and habits can often be difficult to distinguish purely on the basis of subjective observation. The context and history of the motor phenomena provide important diagnostic information.
Stereotypies are repetitive, rhythmical, and invariant motor behaviors, without an apparent purpose or function, that can vary from simple motor behaviors such as rocking or hand waving to extraordinarily complex acts and rituals. They are one of the defining features of autism and are common in patients with mental retardation. Stereotypies are seen in adults with lesions or disorders affecting the frontostriatal circuit running between the dorsolateral frontal cortex and the head of the caudate nucleus. Frontotemporal dementias commonly manifest with stereotypic behaviors resulting from degeneration of the dorsolateral prefrontal cortex. Stimulant medications can produce complex stereotypies through a dopaminergic effect on the basal ganglia. Other repetitive motor behaviors such as compulsive behaviors and tics are seen in patients with Gilles de la Tourette syndrome and obsessive-compulsive disorder, both of which are considered to be associated with basal ganglia pathology. Of importance is that stereotypies, compulsions, complex tics, mannerisms (unusual or pathological styles of performing goal-directed activities, such as a bizarre gait and unusual ways of greeting people), and habits can often be difficult to distinguish purely on the basis of subjective observation. The context and history of the motor phenomena provide important diagnostic information.
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