The Effects of an Occipital Lobe Stroke

Occipital lobe infarctions are different

The Effects of an Occipital Lobe Stroke

We hypothesized that occipital lobe infarctions differ from infarctions in other locations as to etiology, risk factors and prognosis among young adults.

Location, etiology, risk factors and long-term outcome were evaluated among all young adults 15–49 years suffering from cerebral infarction in Hordaland County, Norway between 1988 and 1997.

The following variables were more frequent among patients with occipital lobe infarction compared with patients with infarctions located elsewhere: younger age (P < 0.001), female sex (P = 0.016), prothrombotic state (P = 0.005) and lack of hypertension (P = 0.001). There was no difference as to long-term mortality or recurrence of cerebral infarction.

Occipital lobe infarctions differ from infarctions in other locations among young adults. This may have important etiologic and therapeutical implications that need further studies.

Keywords: cerebral infarction, occipital lobe, young adults

It has been shown in a number of studies that the distribution of etiology of cerebral infarction among young patients differs from the distribution among older patients (Adams et al 1993; Naess et al 2004). Further, it has been shown that the long-term prognosis among young patients with cerebral infarction differs as to etiology and risk factors (Naess et al 2005).

These differences may have important therapeutic implications. It is possible that different locations of the brain are differently susceptible to various etiologies of cerebral infarction.

Thus, we hypothesized that infarctions in the occipital lobe differ as to the distribution of etiology, risk factors and the long-term prognosis compared with infarctions located in other parts of the brain.

Patients 15–49 years old suffering from a first-ever cerebral infarction from 1988 to 1997 and living in Hordaland County, Norway for at least 5 years before the stroke occurred were included. Cases were found by computer search from hospital registries at each of the five hospitals in the county.

The search criteria were patients 15–49 years old admitted to an inpatient or outpatient department of one of the hospitals from 1988 to 1997 (10 years) and discharged with a diagnosis of primary or secondary stroke: categories 430–438 of the International Classification of Diseases, ninth revision (ICD-9).

Cerebral infarction was defined in accordance with the Baltimore-Washington Cooperative Young Stroke Study Criteria comprising neurological deficits lasting more than 24 hours because of ischemic lesions, or transient ischemic attacks where computed tomography (CT) or magnetic resonance imaging (MRI) showed infarctions related to the clinical findings (Johnson et al 1995). We excluded patients with cerebral infarction associated with other intracranial diseases such as subarachnoidal hemorrhage, sinus venous thrombosis, or severe head trauma.

Hypertension was defined as treatment with antihypertensive drugs before stroke onset or the introduction of antihypertensive treatment before discharge because of repeated blood pressure measurements >140/90 mmHg.

Diabetes mellitus was considered present if it was diagnosed before stroke onset (patient on glucose-lowering diet or medication) or during the hospital (fasting plasma glucose >7.7 mmol/L several days after stroke onset). Current smoking at stroke onset was defined as smoking at least one cigarette per day.

Angina pectoris and myocardial infarction were considered present if diagnosed by a physician any time before stroke onset. The presence of migraine was self-assessment.

The diagnostic work-up comprised CT, MRI, electrocardiography, echocardiography, Doppler sonography of extra- and intra-cranial arteries, conventional angiography, and laboratory studies including complete blood cell count, electrolytes, creatinine, glucose, cholesterol, protein C, protein S, antithrombin III, anticardiolipin antibodies, lupus anticoagulant, and homocysteine. Causation was the TOAST (Trial of Org 10172 in Acute Stroke Treatment) criteria (Adams et al 1993).

All surviving patients were invited to a follow-up visit. Information on recurrence of cerebral infarction and post-stroke myocardial infarction was self-report and review of all patient records.

Blood samples were drawn at follow-up for determination of total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL). A total of 199 (95.

2%) of all surviving patients came to the follow-up control.

Independent samples T-test and Fisher’s exact test were used when appropriate. Multivariate analysis was made using occipital lobe infarction (OLI) or extra-occipital lobe infarction (ELI) as dependent variable. The analyses were performed with SPSS 11.0.1 for Windows.

The total patient population comprised 136 men (59%) and 96 women (41%). Nineteen (8.2%) patients had OLI and 213 (91.8%) patients had ELI. Table 1 shows the demography of OLI and ELI patients. OLI patients were younger (P < 0.001) and more frequent female (P = 0.016). None of the OLI patients had hypertension (P = 0.001).

There were no differences as to diabetes mellitus, smoking, migraine and coronary heart disease. Systolic and diastolic blood pressures on admittance were significantly lower among the OLI patients. CT was negative among 39.6% ELI patients and 26.3% OLI patients (P = 0.497). A prothrombotic state was present among 26.

3% OLI patients and 5.2% ELI patients (P = 0.005). Among OLI patients the prothrombotic state included pregnancy (n = 2), antithrombin III deficiency (n = 2), and polycytemia vera (n = 1).

Among ELI patients the prothrombotic state included pregnancy (n = 2), post-partum state (n = 2), protein S deficiency (n = 2), lupus anticoagualant (n = 1), thrombocytopenic purpura (n = 1), and systemic lupus erythematosus (n = 1).

The only OLI patient with stroke of other determined cause had mitochondrial encephalomyopathy, lactic acidosis, and stroke- episodes (MELAS). Stroke of other determined cause among 3 ELI patients included homocysteinemia, Conn’s syndrome and Borrelia-related arteritis.

Demography of young adults with occipital infarctions compared with infarctions other than occipital)

Occipital infarctions %Other infarctions %P
Male31.660.80.016
Mean age (years)33.542.3

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291333/

When Stroke Affects the Occipital Lobe

The Effects of an Occipital Lobe Stroke

The occipital lobe of the brain is located at the back of the head and is named for the occipital bone that covers it (Latin ob, behind, and caput, the head). It is the smallest of the four lobes of the cerebral cortex, and it’s pretty much a one trick pony. But that one trick — vision — is an important one.

When we look at something, that visual stimuli are sent along the optic nerves, which run the length of the brain all the way to the occipital lobe, which processes that visual information for us.

“The occipital lobe has two hemispheres, and just the other lobes in the brain, each control the opposite side of the body,” said neurologist Elisabeth Marsh, associate professor of neurology at the Johns Hopkins School of Medicine.

For both of our eyes, the left side of the occipital lobe is responsible for what we see in the right side of our field of vision — and the right side of the occipital lobe, for the left side of our field of vision.

In other words, the left hemisphere doesn’t control the right eye, it processes visual stimuli for the right side of each eye.

That fact leads to quite a vexing stroke deficit, and the most common visual deficit — a field cut (homonymous hemianopsia) where a person sees only half the world. Unfortunately, a field cut is often misinterpreted as a problem with the eye.

“When people come to my clinic and say, ‘I can’t see my right eye,’ my first job as a neurologist is to confirm that’s truly the case,” Marsh said.

“‘Is it really your eye you can’t see ? What happens when you close the eye you think is the problem?’ If their vision becomes normal, then it really is the eye that’s the problem. But more commonly, people close the eye and realize they still can’t see on one side of space. The same deficit affecting both eyes is a brain, or more specifically, an occipital lobe problem.”

It's Not Just the Eyes

Dr. Elisabeth Marsh

We often limit vision to our eyes, but vision is really an additive process. Impulses from the retina travel along the optic tracts to the occipital lobe where they are processed.

“There are discrete areas within the occipital lobe that are responsible for different parts of your vision,” Marsh said. For instance, motion is detected in a separate place in the occipital lobe than pattern recognition.

Some parts of the occipital lobe identify movement, or color, or even the different parts of an object that make up the whole.”

But after the occipital lobe processes vision, the rest of the brain is important for actually perceiving and figuring out what that means.

“After vision gets processed in the occipital lobe, the movement and patterns have to be perceived, which is done in the parietal lobe,” she said.

“Then how one responds to the stimulus, how they feel about what they’re seeing, is determined in the temporal lobe. In other words, the entire brain is important for processing that visual stimuli, but it starts with the occipital lobes.”

Marsh pointed out that recognizing the difference between a field cut and neglect, a common stroke deficit involving inattention, can be difficult: “If someone is not seeing that side of space, sometimes it can be hard to tell whether their attention there is good or not. But neglect tends to be more of a temporoparietal [controlled by the temporal and parietal lobes] function in general. These two syndromes can be difficult to differentiate in patients,” she said.

Blood Flow

Most of the occipital lobe’s blood flow is from the artery in the back of the brain (posterior cerebral artery or PCA).

However, the middle cerebral artery (MCA) supplies a small portion of the occipital lobe.

“That part is the center of the vision called the macula, which is good because if you have a sizable PCA stroke, sometimes the macula and the central vision can be spared,” Marsh said.

Marsh says that strokes in the PCA are less common than those in the MCA. The PCA has more twists and turns, so clots tend to travel the easier path of the MCA. “But certainly, PCA strokes are not infrequent,” she said.

“Two types of disease result in PCA strokes. One is cardiac disease, more specifically, atrial fibrillation (AFib). When a patient is in AFib, blood can pool in the heart and form clots that then travel to the brain and lodge in the big blood vessels the PCA.

The other major stroke type leading to occipital lobe strokes is large vessel disease, where lipid plaques form due to vascular risk factors hypertension [high blood pressure], hyperlipidemia, and smoking, that can result in a stroke of the occipital lobe.”

There is also a difference between ischemic strokes and hemorrhagic strokes. “Ischemic strokes tend to obey vascular borders. The neurons fed by the PCA are the ones affected when a clot blocks blood flow through the vessel.

With a hemorrhagic stroke, there’s rupture of the vessel so these borders are disrupted, and in addition there can be swelling that expands the territories involved. Patients may be weak or have aphasia because of all the edema.

How Some Visual Field Cuts May Appear To Stroke Survivors

For more examples of field cuts, see our From the Eyes of the Beholder infographic.

Hallucinations

With field cuts, the survivor typically can’t see what’s there, but occipital lobe strokes can produce the opposite effect — seeing something that is not there. That can be for two reasons.

“First, it can be because you have cells that are injured and malfunction, resulting in seeing lights or zigzags,” Marsh said. “But in addition, the brain is really smart and knows it’s supposed to be seeing something.

It doesn’t it when it’s not getting the input it expects, so it starts to make things up to fill in the gaps. This can actually happen with occipital lobe strokes or any cause of visual impairment, such as macular degeneration.

Most commonly, people will detect movement and then perceive that those movements are performed by people. Hallucinations can be quite complex.”

These kind of vivid hallucinations, called the Charles- Bonnet syndrome, apparently are rare, but Marsh says it is hard to know precisely.

“People who experience them may think they are crazy, so they don’t talk about it unless prompted,” she said.

“Whenever anybody has a visual problem, I always ask if they’re seeing things that they know aren’t there? If you bring it up carefully, you can often get them to open up and then reassure them.”

Confusion

The thalamus and brainstem can also be affected with an occipital lobe stroke. The vessel that supplies the PCA, which supplies both the occipital lobe and the thalamus, is the basilar artery, which also feeds the brainstem. It’s not uncommon for a clot traveling up the basilar to break up and affect multiple locations.

A stroke that affects both the thalamus and the occipital lobe can produce a second deficit — confusion.

“It’s not uncommon for people to not only present with a visual problem but also with confusion when they have a PCA stroke,” Marsh said. “It’s not that they are unable speak, they’re not aphasic.

But they’re often confused, and families will say that they’re ‘not right,’ not behaving the way they normally do.”

Compensating For Deficits

Therapy and recovery from occipital lobe stroke can be difficult. Occipital lobe strokes don’t impact the ability to move, nor are they ly to produce aphasia. This leads many people to think the survivor got off lucky, with “minor deficits.”

“But when you talk to people who have had an occipital lobe stroke and can’t see half of their visual field, it’s a very big deal,” Marsh said. “Not being able to see on one side of space means you can’t drive, which takes away independence.

Depending on what you do, a field cut can also affect one’s ability to work. For instance, I have a patient who’s a welder and can’t go back to operating heavy machinery because it would be unsafe.

Strokes resulting in vision problems can be devastating.”

Whereas rehabilitation can often help survivors with weakness or movement problems recover some of their previous function, survivors with visual deficits are far less ly to recover any of their vision.

“Unfortunately, once those neurons are lost, there’s no getting them back, and the opposite hemisphere can’t take over the function” she said.

“However, occupational therapy can teach a patient how to compensate for their deficit and become quite functional.”

Emotional Challenges

The occipital lobe doesn’t have an operational role in emotions or executive function, but Marsh pointed out, “Having a stroke itself changes the brain chemistry and makes post-stroke depression far more ly.”

This information is provided as a resource to our readers. The tips, products or resources listed or linked to have not been reviewed or endorsed by the American Stroke Association.

Source: http://strokeconnection.strokeassociation.org/Fall-2019/When-Stroke-Affects-the-Occipital-Lobe/

Anton’s Syndrome due to Bilateral Ischemic Occipital Lobe Strokes

The Effects of an Occipital Lobe Stroke

We present a case of a patient with Anton’s syndrome (i.e., visual anosognosia with confabulations), who developed bilateral occipital lobe infarct. Bilateral occipital brain damage results in blindness, and patients start to confabulate to fill in the missing sensory input.

In addition, the patient occasionally becomes agitated and talks to himself, which indicates that, besides Anton’s syndrome, he might have had Charles Bonnet syndrome, characterized by both visual loss and hallucinations. Anton syndrome, is not so frequent condition and is most commonly caused by ischemic stroke.

In this particular case, the patient had successive bilateral occipital ischemia as a result of massive stenoses of head and neck arteries.

1. Introduction

Visual anosognosia, or denial of loss of vision, which is associated with confabulation in the setting of obvious visual loss and cortical blindness is known as Anton’s syndrome [1].

Originally, the syndrome is named by Gabriel Anton, who described patients with objective blindness and deafness showing a lack of self-perception of their deficit. Later Joseph Babinski used the term anosognosia to describe this phenomenon [2, 3].

Bilateral occipital brain damage results in blindness; however, patients start to confabulate to fill in the missing sensory input.

Why patients with Anton’s syndrome deny their blindness is unknown, although there are many theories. Although visual anosognosia is frequently believed to represent cortical phenomenon, it is probably more often caused by parietal white matter injury leading to a disconnection syndrome [4, 5].

In this paper, we present a case of patient with Anton’s syndrome due to bilateral occipital ischemic lesions as a result of massive stenoses of head and neck arteries.

2. Case Presentation

A 76-year-old man has been admitted to the Neurology Department of University Clinical Center Tuzla due to a sudden and moderate paresis of the left hand and left leg and impaired speech with dysarthria and without elements of anosognosia or unilateral neglect.

Previous medical history revealed longstanding hypertension, diabetes, and atrial fibrillation. The Glasgow coma scale (GCS) score was 15 15. Neurological examination revealed left homonymous hemianopsia, central type facial palsy, and paresis of left extremities. He was eupneic, afebrile, and hypertensive.

He also had a systolic murmur over the right carotid artery.

Color Doppler of the neck vessels performed immediately after the admission showed a complete occlusion of the left internal carotid artery (ICA) and left vertebral artery (VA), also moderate stenosis of the right ICA and significant stenosis of the right VA, with atherosclerotic plaques on all other blood vessels.

Urgent computed tomography (CT) of the brain revealed an ischemic lesion in the right temporooccipital region (Figure 1). Soon after the admission, the patient develops a new neurological deficit of right sided paresis. Follow-up CT scans revealed a newly developed left occipital acute ischemia (Figure 2).

CT angiography confirmed the ultrasound findings along with an incipient stenosis of the left subclavian artery. The right posterior cerebral artery showed a gracile flow with narrowing in the middle of the artery (Figure 3), with atherosclerotic changes in the remaining blood vessels of the head and neck.

Newly developed neurological deficit also included a gradual loss of vision, due to bilateral occipital lesion. Ocular movements and pupillary reflexes were intact suggesting that anterior visual pathways were not damaged. Fundoscopy was unremarkable. The patient was not aware of the sight loss.

In particular, the sight loss was observed for the first time when the patient asked for a door to be opened, even though the door was already standing wide open. When asked about the position of the door, the patient pointed to the obviously wrong direction.

Also when asked to describe the attending physician, the patient provided a completely wrong visual description of the physician. In addition, he was unable to reach physician’s extended hand.

Despite this obvious blindness, the patient suffered a visual anosognosia, since he was unaware of his blindness and was confabulating about his surroundings when asked about it. Complete blindness was confirmed by ophthalmologist due to an absence of response to simulation of visual evoked potentials (Figure 4).

The patient adamantly claimed he was able to see, despite the confirmed blindness test. Furthermore, medical staff reported that he would occasionally become agitated and talk to himself. Consequently, the patient has been treated with clopidogrel, antihypertensive, antidiabetic, and statin drugs.

The drugs treatment, together with physical and speech therapy, results in an improvement of reduction in neurologic deficit. However, at the time of discharge, persistent elements of Anton’s syndrome were present. The patient has been followed up as an outpatient, having a neurological improvement and being able to walk with minor help. Blindness remained permanent. One year later the patient deceased due to cardiovascular complications.

3. Discussion

Bilateral occipital stroke is a common cause of visual anosognosia also known as Anton’s syndrome [6]; however, consecutive occipital strokes as a cause of Anton’s syndrome are rather uncommon.

In our patient, at admission CT of the brain revealed only ischemic lesion in the right temporooccipital region, but soon after the admission an ischemic lesion in the left occipital region has developed.

Cortical blindness due to bilateral damage of the occipital lobes was most ly secondary to hypoxia, vasospasm, and cardiac embolism [7].

Confabulation is one of the important criteria of Anton’s syndrome. Anton suggested that damaged visual areas are effectively disconnected from functioning areas, such as speech and language areas. In the absence of input, functioning speech areas often confabulate a response [1, 8].

Our patient showed all aspects of Anton’s syndrome, visual anosognosia, and confabulation. However, medical staff also reported that he would occasionally become agitated and talk to himself, which may indicate that he might have had Charles Bonnet syndrome, characterized by both visual loss and hallucinations [9].

Bilateral cortical blindness and Anton syndrome are most commonly caused by bilateral occipital lobe lesions [1, 5, 10]. This syndrome was also reported in a few other medical conditions such as gynecological complications (preeclampsia and obstetric hemorrhage) [11], MELAS [12], trauma [13], adrenoleukodystrophy [14], hypertensive encephalopathy [15], and angiographic procedures [16].

Considering that recovery of visual function depends on the underlying etiology, in this case we could not expect the full recovery mainly because of multiple stenoses of head and neck arteries. Patient was not considered for surgical treatment because of age and other risk factors. Therefore, management was focused on secondary prevention and rehabilitation.

4. Conclusion

We should suspect Anton’s syndrome (visual anosognosia), when the patient has denial of blindness with evidence of occipital lobe damage, or even the Charles Bonnet syndrome, which is comprised of both the visual loss and hallucinations.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.

Copyright © 2014 Sanela Zukić et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Source: https://www.hindawi.com/journals/crinm/2014/474952/

Occipital Lobe Stroke: Understanding Vision Problems, and More

The Effects of an Occipital Lobe Stroke

A stroke in the occipital lobe often results in visionproblems since this area of the brain processes visual input from the eyes.

Aside from visual deficits, occipital lobe strokes alsocause unique stroke symptoms that you should learn to recognize in order tohelp save a life.

Here’s everything you should know about occipital lobestroke – also known as occipital lobeinfarct.

Cause of Occipital Lobe Stroke

A strokeoccurs when the supply of blood in the brain becomes blocked by either aclogged or burst artery.

When a blood clot clogs an artery in the brain, it’s knownas an ischemic stroke, which accounts for 87%of all strokes. A burst or ruptured artery, on the other hand, is known as ahemorrhagic stroke.

When part of the brain becomes deprived of oxygen-rich blooddue to stroke, brain cells begin to die. This can create serious complications,making stroke a medical emergency that requires immediate, swift treatment.

Treatment for Occipital Lobe Stroke

Once occipital lobe stroke patients arrive in the hospitalfor treatment, doctors may use of clot-busting drugs, tPA or aspirin, to restoreblood flow in the brain after an ischemic stroke.

Hemorrhagic strokes often require more invasive treatment surgery (craniotomy) to stop the bleeding and relieve pressure within the skull.

Before we get to the side effects and rehabilitation foroccipital lobe stroke, it’s important to know how the symptoms vary from otherstrokes.

Symptoms of Occipital Lobe Stroke

Typically, strokes can be identified using the acronym “FAST,”which includes:

  • Facialdrooping, where one side of the face sags downward
  • Armweakness, where one arm cannot be lifted as high as the other
  • Slurredspeech, where the person cannot talk normal
  • Time –where time is of the essence for treatment!

However, it’s critical to note that a stroke in theoccipital lobe often presents unique symptoms,such as:

  • Visual disturbancessuch as partial or complete blindness or hallucinations
  • Severe headacheor migraine that lasts longer than usual (25% of strokes areaccompanied by headaches)
  • Tinglingon one or both sides of the body
  • Numbness
  • Lightheadedness

If you ever encounter these symptoms, call 9-1-1 right awayfor emergency treatment. Time is brain, and swift action can help save a life!

Once a stroke has been identified and treated, patients mustwork to overcome the side effects that may occur.

Occipital Lobe Stroke Deficits

The primary stroke deficit that occurs after an occipitallobe stroke involves vision problems.

There are manyways that vision can be affected after an occipital lobe stroke.

Here are the different types of vision problems afteroccipital lobe stroke:

  • Homonymous hemianopia. The occipital lobe spans across both hemispheres of the brain. When stroke affects the occipital lobe on one side, it can cause blindness on the opposite side of the visual field. For example, a stroke in the right occipital lobe can result in blindness on the left side of the visual field.
  • Cortical Blindness. When all vision is lost after an occipital lobe stroke, it’s called cortical blindness. This differs from “regular” blindness because the eyes are unaffected, but the visual processing abilities of the brain have been severely compromised.
  • Central vision loss. When a stroke affects the occipital pole (the area of the occipital lobe that processes central vision), patients may experience blindness in the middle of their visual field. They can see in their peripheral, but not directly in front of them.
  • Visual Hallucinations. In rare cases, an occipital lobe stroke can result in vivid hallucinations where patients see various images lights, sparks, colorful pinwheels, etc.
  • Prosopagnosia. This refers to “face blindness” where the patient cannot recognize faces. This may occur when the part of the occipital lobe that processes faces has been impacted by the stroke. (This is also common in right hemisphere strokes.)
  • Visual Agnosia. This occurs when the patient cannot identify familiar objects and/or people by sight.
  • Alexia without Agraphia. Alexia refers to inability to read or understand written word. Agraphia refers to the inability to communicate through writing. Therefore, an occipital lobe stroke may impact a patient’s ability to read or understand word by looking at the word – it’s a visual problem, not a language problem.

Aside from vision, some occipital lobe stroke patients mayalso experience sensory issues such as numbnessor tinglingsensations.

However, when stroke only affects the occipital lobe, studies have reportedthat patients often have “no significant neurological deficits other thanvisual-field loss.”

If the stroke impacted more than just the occipital lobe,then otherstroke side effects may occur as well.

Rehabilitation for Occipital Lobe Stroke

With most side effects of occipital lobe stroke involvingvision problems, rehabilitation will revolve around restoring eyesight.

Talk to your doctor, who can refer you to a neuro-ophthalmologist or neuro-optometrist. It’s important to see specialists who understand the neurological impact of the stroke on visual processing. A regular optometrist may not be able to help.

After seeing a specialist, some treatment plans may include vision restoration therapy. These therapies capitalize on neuroplasticity after stroke, which involves the brain’s ability to heal itself and form new neural networks.

Organizations PlasticityBrain Centers specialize in programs that can help you rebuild theeye-brain connection. Some modalities used include eye movement training (eyeexercises), hand-eye coordination exercises, or light therapy.

Vision is important for carrying out the activities of dailyliving, so it’s important to exercise caution and work with trained specialistswhen your vision has been affected by stroke.

Outlook for Occipital Lobe Stroke

Participation in rehabilitation is encouraged to capitalizeon the brain’s ability to heal itself, especially during the first 3 monthsafter stroke.

Some patients may experience spontaneous recovery wheretheir vision returns naturally. According to Healthline,this may take around 6 months, but it varies from person to person becauseevery stroke is different.

Overall, there is hope for recovery from occipital lobestroke. By working closely with your medical team, you can come up with arehabilitation plan that will help you navigate your new life after stroke.

Best of luck on the road to recovery.

Source: https://www.flintrehab.com/2019/occipital-lobe-stroke/

Occipital Brain Lobe and Its Function

The Effects of an Occipital Lobe Stroke

The occipital lobe participates in vision processing. It processes and interprets everything we see. The occipital lobe is also responsible for analyzing contents, such as shapes, colors, and movement, and also for interpreting and drawing conclusions about the images we see.

Boundaries, Anatomy, Position, and Structure of the Occipital Brain Lobe

The boundaries of the occipital lobe include the edges of the parietal and temporal lobe. The occipital lobe contains the primary visual cortex and associative visual areas (1).

The occipital lobe occupies the posterior parts of the hemispheres. On the convex surface of the hemisphere, the occipital lobe has no sharp boundaries separating it from the parietal and temporal lobes.

The exception is the upper part of the parietal-occipital groove, which, located on the inner surface of the hemisphere, separates the parietal lobe from the occipital lobe. The furrows and edges of the upper canopy of the occipital lobe are unstable and have a variable structure.

On the inner surface of the occipital lobe, there is a groove of spores, which separates the wedge (triangular norm of the occipital lobe) from the lingual gyrus and the occipital-temporal gyrus (1). 

In the occipital lobe of the cerebral cortex is, the following fields are positioned: 

  • Area 17 – Gray matter buildup in a visual analyzer. This field is the primary zone. It is made up of 300 million nerve cells.
  • Area 18 – It is also a nuclear set of visual analyzers. This field performs the function of perceived writing and is a more complex secondary area. 
  • Area 19 – This field is involved in evaluating the value of what we see. 
  • Area 39 – This brain part does not completely belong to the occipital region. This area is located at the border between the parietal, temporal, and occipital lobes. Its functions include integrating visual, auditory, and general sensitivity of information (1).

The Function of the Occipital Brain Lobe

The function of the occipital lobe is related to the perception and processing of visual information, as well as the organization of complex processes of visual perception.

At the same time, the upper half of the retina, which detects light from the lower field of vision, is projected into a wedge; in the reed area, the gyrus is the lower half of the retina, noticing the light from the upper field of view(1).

In the occipital cortex, there is a primary visual area (the cortex of the part of the sphenoid gyrus and the lingual lobule). There is a local representation of the retinal receptors. Each retinal point corresponds to its portion of the visual cortex, while the yellow dot area has a relatively large representation area.

In connection with the incomplete intersection of visual pathways, the same half of the retina is projected into the visual area of each hemisphere. The presence of retinal projection of both eyes in each hemisphere is the basis of binocular vision.

The neurons of these zones are polymodal and respond not only to light but also to tactile and auditory stimuli. Different types of sensitivities are synthesized in this visual area, more complex visual images emerge and they are recognized.

An example can be given to understand the function of the occipital lobe in visual perception. When we look at a map and “put” the route planner information into our working memory, the first step would be to process millions of light stimuli in the recognition centers, i.e. to process different signals perceived by the photosensitive cells of our retina. 

Furthermore, the occipital lobe receives incoming information, which is processed and immediately sent to the hippocampus, where it is formed into memory. Firstly, it becomes short-term memory. Accordingly, we remember the name of the place of destination and remember it as we move along this route.

As we have already stated, the occipital lobe is responsible for the visual perception of information, as well as its operational storage. Generally, everything projected by the retina is recognized and formed into a specific image in the occipital lobe.

For absolutely healthy people, this proportion works independently and flawlessly, but irreparable consequences can occur with injuries and some illnesses. Sometimes, total blindness can occur. This is the process that happens if there is a damage on the surface of the primary visual cortex.

Light signals transmit information to the occipital lobe via nerve endings, which represents a form of irritation or stimuli for the retina. The nerves then transmit information to the diencephalon, another part of the brain. And diencephalon, in turn, sends information to the primary visual cortex, called the sensory cortex.

From the primary sensory cortex, nerve signals are sent to the adjacent areas and are called sensory associative cortex areas. The main function of the occipital lobe is to send signals from the primary visual cortex to the visual associative cortex. The areas described together analyze the visual information observed and retain visual memories. 

As already implied, this occurs when the primary visual cortex, whose surface is visible, is damaged. Complete damage to the primary cortex occurs in three cases, as a result of a head injury, as a result of the development of a tumor on the surface of the brain, and finally, yet very rarely, as a consequence of certain congenital anomalies.

Damage of the Occipital Brain Lobe

Damage to the primary visual cortex leads to a form of central blindness called the Anton’s syndrome; patients cannot recognize objects via their sense of sight and are completely unaware of their deficits (2).

Epileptic seizures in the area of the occipital lobe cause visual hallucinations, most commonly in the form of dashes and a colored mesh that appears on the contralateral field of view.

Damage of the occipital brain lobe can occur as a result of a head injury, a tumor on the surface of the brain, and certain congenital anomalies. 

However, focal lesions do not lead to complete loss of vision. For example, after taking a familiar object in his hands, a patient may describe the object he/she is touching. However, if that same object is shown in the picture, then the patient will not be able to describe its shape and color. In medical language, this condition is called visual agnosia. 

At times, focal lesions can localize and restore vision and perception. However, it is important to note that the chances of a partial recovery in children are higher than those in patients whose brain is already formed and not growing anymore. Treatment is usually done surgically(2).

Pain in the occipital brain lobe region

There are many different causes of pain in this region. Some of them include:  

  • Nerve tension and stress. With prolonged tension, neck and back muscle spasms and neck pain occurs. Also, pain in the occipital brain region can be localized. The patient can diminish the pain by breathing calmly and deeply. If the pain does not stop after the patient feels relaxed, a visit to a doctor is obligatory. 
  • Osteochondrosis of the cervical spine. This condition results in sharp pain in the back of the head. Specialized forms of gymnastics can help. However, the patient must see a neurologist. 
  • High blood pressure. This condition can cause pain with a feeling of fullness. Pressure control is essential for extending one’s lifetime. Contact a neurologist if you feel pain in the occipital part of your brain and suffer from blood pressure disorders. 
  • Increased intracranial pressure. This serious condition is characterized by oppressive eye pain. The pain is localized in the occipital lobe. The patient must immediately see a doctor.

Conclusion

The occipital lobe is located in a triangle, the apex of which is the parietal lobe and the sides of the temporal lobes of the brain. The cerebellum is positioned below the occipital lobe. This brain part has a variable structure.

Its key function is processing visual information. The visual cortex, located on both hemispheres of the occipital lobe, provides binocular vision – the world seems vast and wide to the human eye. 

The visual cortex, called the associative area, constantly communicates with other brain structures, forming a complete image of the world. The occipital lobe has strong links with the limbic system (especially the hippocampus), the parietal, and temporal lobes.

Thus, this or that visual image may be accompanied by negative emotions or vice versa: long-term visual memory may evoke positive emotions.

The occipital lobe, along with simultaneous signal analysis, also plays the role of an information container. However, the amount of such information is insignificant, and most of the environmental information is stored in the hippocampus.  

The occipital cortex is strongly associated with feature integration. The essence of these theories is that the cortical analytic centers of separate properties of an object (color) are processed separately, and in parallel with the processing of other information.

To sum up, the occipital lobe is responsible for processing visual information and their integration into the general relation to the world; storing visual information; interaction with other areas of the brain, and, partly, tracking their functions; as well as the binocular perception of the environment.

References:

Source: https://human-memory.net/occipital-brain-lobe/