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Focal cerebral ischemia differs fundamentally from global ischemia In the latter state, if absolute, there is no cerebral blood ow of the entire brain and irreversible destruction of neurons occurs within 4 to 8 min at normal body temperature In focal ischemia, there is nearly always some degree of circulation (via collateral vessels), permitting to a varying extent the delivery of oxygenated blood and glucose The effects of a focal arterial occlusion on brain tissue also vary depending on the location of the occlusion in relation to available collateral and anastomotic channels If the obstruction lies proximal to the circle of Willis (toward the heart), the anterior and posterior communicating arteries of the circle are often adequate to prevent infarction In occlusion of the internal carotid artery in the neck, there may be anastomotic ow from the external carotid artery through the ophthalmic artery or via other smaller externalinternal connections (Fig 34-2) With blockage of the vertebral artery, the anastomotic ow may be via the deep cervical, thyrocervical, or occipital arteries or retrograde from the other vertebral artery If the occlusion is in the stem portion of one of the cerebral arteries, ie, distal to the circle of Willis, a series of meningeal interarterial anastomoses may carry suf cient blood into the compromised territory to lessen (rarely to prevent) ischemic damage (see Figs 34-2 and 34-3) There is also a capillary anastomotic system between adjacent arterial branches, and although it may reduce the size of the ischemic eld, particularly of the penetrating arteries, it is usually not signi cant in preventing infarction Thus, in the event of occlusion of a major arterial trunk, the extent of infarction ranges from none at all to the entire vascular territory of that vessel Between these two extremes are all degrees of variation in the extent of infarction and its degree of completeness Additional ischemia-modifying factors determine the extent of necrosis The speed of occlusion assumes importance; gradual narrowing of a vessel allows time for collateral channels to open The level of blood pressure may in uence the result; hypotension at a critical moment may render anastomotic channels ineffective Hypoxia and hypercapnia are presumed to have deleterious effects Altered viscosity and osmolality of the blood and hyperglycemia are potentially important factors but dif cult to evaluate Finally, anomalies of vascular arrangement (of neck vessels, circle of Willis, and surface arteries) and the existence of previous vascular occlusions must in uence the outcome The speci c neurologic de cit obviously relates to the location and size of the infarct or focus of ischemia The territory of any artery, large or small, deep or super cial, may be involved When an infarct lies in the territory of a carotid artery, as would be expected, unilateral signs predominate: hemiplegia, hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences In the territory of the basilar artery, the signs of infarction.

tie %db, 'GDBM_File', 'databasedb', O_CREAT|O_RDWR, 0644;

Vertebral A Angular A R subclavian A Deep cervical A Thyrocervical A Innominate A Aortic arch Lacrimal A

J:(b-tt)

You will need the definitions from the Fcntl module for the specification of the different flags when opening and closing the files The different flags available for all DBM implementations are shown in Table 13-2 Both GDBM and Berkeley DB have their own additional flags, which we will examine separately Once opened, the DBM file can be accessed using the hash it has been tied to For example, the following code fragment opens a text file and creates a DBM database of the contents The first line of the text file is assumed to be the list of fields to be used as keys in the rest of the database

Figure 34-2 Arrangement of the major arteries on the right side carrying blood from the heart to the brain Also shown are collateral vessels that may modify the effects of cerebral ischemia For example, the posterior communicating artery connects the internal carotid and the posterior cerebral arteries and may provide anastomosis between the carotid and basilar systems Over the convexity, the subarachnoid interarterial anastomoses linking the middle, anterior, and posterior cerebral arteries are shown, with insert A illustrating that these anastomoses are a continuous network of tiny arteries forming a border zone between the major cerebral arterial territories Occasionally a persistent trigeminal artery connects the internal carotid and basilar arteries proximal to the circle of Willis, as shown in insert B Anastomoses between the internal and external carotid arteries via the orbit are illustrated in insert C Wholly extracranial anastomoses from muscular branches of the cervical arteries to vertebral and external carotid arteries are indicated in insert D

i- 135

Appends information to the given file Creates a new file if it doesn t already exist Causes the open to fail if the file already exists when used with O_CREAT Opens the file without blocking; reads or writes to the file will not cause the process to wait for the operation to be complete Behaves as O_NDELAY Opens the file read-only Opens the file for reading and writing Opens the file, truncating (emptying) the file if it already exists Opens the file write-only

leading invariably to histologic signs of necrosis These changes do not become apparent for several hours Free fatty acids (appearing as phospholipases) are activated and destroy the phospholipids of neuronal membranes Prostaglandins, leukotrienes, and free radicals accumulate, and intracellular proteins and enzymes are denatured Cells then swell, a process called cellular, or cytotoxic, edema (see page 550) Similar abnormalities affect mitochondria, even before other cellular changes are evident

j:2,46

O_NONBLOCK O_RDONLY O_RDWR O_TRUNC O_WRONLY Table 13-2

Implicit in all discussions of ischemic stroke and its treatment is the existence of a penumbra zone that is marginally perfused and contains viable neurons Presumably this zone exists at the margins of an infarction, which at its core has irrevocably damaged tissue that is destined to become necrotic Using various methods, such a penumbra can be demonstrated in association with some infarctions but not all, and the degree of reversible tissue damage is dif cult to determine The neurons in the penumbra are consid-

13:

fG)+f(r,,)

Basilar A Penetrating branches of middle cerebral A A1 segment, anterior cerebral artery M1 segment, middle cerebral artery Posterior cerebral A (P1 segment) Superior cerebellar A Short circumferential A Paramedian arteries 5th N 6th N 7th N 8th N Anterior inferior cerebellar A D 12th N B C Mid-pontine 2 mm above pontomedullary junction 6 mm below pontomedullary junction 3rd N A 4 mm below upper border of pons

#!/usr/local/bin/perl5 -w use NDBM_File; use Fcntl; my ($dbfile,%db,$i,@fieldnames,@fields,$key,$n); die "Usage:\n$0 source\n" if (@ARGV<1); $dbfile = $ARGV [0]; PROGRAMMING WITH PERL open(D,"<$dbfile") || die "Can't open $dbfile, $!"; (tie %db, NDBM_File, $dbfile, O_RDWR|O_CREAT|O_EXCL, 0666) || die "$0: Error creating $dbfile: $!\n"; $_ = <D>; chomp; s/,//; @fieldnames = split "\t"; $db{fieldlist} = join(",",@fieldnames); while(<D>) { chomp; @fields = split "\t"; for($n=0;$n<=@fields;$n++) { if (defined($fields[$n])) { $key = $fieldnames[$n] "-$i"; $db{$key} = $fields[$n]; } } $i++; } $db{seqid} = $i; close(D) || die "$0: Couldn't close source, $!\n"; untie %db || die "$0: Couldn't close db, $!\n";