Lyme and the Limbic System
When Stage 3 Lyme begins to attack the brain, the Limbic System is often affected. To better understand the brain, including the Limbic system, enables the Lyme sufferer to better TREAT.
The Limbic System
Limbic is an odd Latin term meaning the edge or border. It’s where we get the word “limbo”. It’s an intermediate state between two important places. Early anatomists saw this area of the brain, that which is between the important neocortex and the midbrain as the ‘in-between area’, or limbic lobe. The limbic system includes one of the following on each side: the hippocampus, amygdala, and other named structures in the temporal lobes that we won’t be discussing. (Some experts would also include parts of the hypothalamus, thalamus, midbrain reticular formation, and olfactory areas in the limbic system.)
Are you bored yet? Hang in there as you may spot some relevance as we discuss symptoms when these structures aren’t working well. The Limbic System houses several important structures to anyone with behavioral or emotional issues.
First let’s discuss the hippocampus because it has such a groovy name. Historically, the earliest hypothesis was that the hippocampus was involved in the sense of smell. Now we know that it is more tied to memories of different smells and how a particular smell of let’s say German potato salad instantly connects us to Grandma’s house on Thanksgiving when you were 5. Over the years, anatomists have whittled down several main ideas of hippocampal function: inhibition, memory, special order, and circadian rhythm.
The behavioral inhibition theory (caricatured by O’Keefe and Nadel as “slam on the brakes!”) was very popular up to the 1960s. It derived much of its justification from two observations: first, that animals with hippocampal damage tend to be hyperactive; second, that animals with hippocampal damage often have difficulty learning to inhibit responses that they have previously been taught.
The second major theory relates the hippocampus to memory. This idea stems from a famous report by Scoville and Brenda Milner describing the results of surgical destruction of the hippocampus (in an attempt to relieve epileptic seizures), in a patient named Henry Gustav Molaison, known until his death in 2008 as H.M. The unexpected outcome of H.M.’s surgery was a specific type of amnesia: H.M. was unable to form new memories after his surgery and could not remember any events that occurred just before his surgery. He retained memories for things that happened years earlier, such as his childhood. This case produced such enormous interest that H.M. reportedly became the most intensively studied medical subject in neurological history.
There were then other patients with similar levels of hippocampal damage and amnesia (caused by accident or disease) have been studied as well. There is now almost universal agreement that the hippocampus plays some sort of important role in memory and most agree its role is more similar to the part of the brain that the original anatomists placed it than they could ever imagine because it is a ‘check station’ for working memory (things happening now) to pass through to long-term storage (in the temporal lobe).
What does this mean to ME?
What does this mean to you? Well, if you’ve ever walked into a room and asked yourself that stupid question, “What did I come in here to get?” then you’ve experienced a “blip” in your hippocampus. Working memory, or current thoughts and plans, needs to shunt back from the planning centers in the prefrontal cortex, through the hippocampus to the temporal lobe where they are stored for future use. “Honey, will you get me the scissors in the kitchen,” spoken when I’m in the middle of writing a section on the limbic system ends up with me standing in the kitchen with absolutely NO idea of why I was there. In this case, brain chatter caused incomplete processing of frontal lobe commands.
Is it just age that brings about a greater incidence of “senior moments”? If so, then somebody tell me why my teenager can’t seem to follow simple instructions even if I tattooed them on her arm. Yes, chatter, disinterest, and not really paying attention will cause working memory issues but abnormal attention problems and continually forgetting where you placed your keys or having to depend more on lists than ever before are all signs of hippocampal damage, most commonly caused by inflammation. We’ll talk more about causes in a later chapter but right now, let’s just admit we may have a problem.
The third important theory of hippocampal function relates the hippocampus to space. The spatial theory was championed by a very influential book, ”The Hippocampus as a Cognitive Map”. As with the memory theory, there is now almost universal agreement that spatial coding plays an important role in hippocampal function. A cognitive map is a type of mental representation (you could say your ‘mind’s eye’) which serves an individual to acquire, sort, store, recall, and decode information about the relative locations (where) and attributes (what) of phenomena in their everyday spatial environment.
You could say that the hippocampus works to sort experiences into respective files and then recover them for future use like a file clerk carefully labeling those little plastic tabs that go on the green hanging files and systematically placing all the important papers in the perfect alphabetical order. Boy, am I dating myself! Maybe a better example would be how I acted just like a hippocampus this morning when I sorted all my Word documents into neat files on my desktop so I wouldn’t have to spend 45 minutes trying to find a handout on liver/gallbladder flush to give to a patient (like I did yesterday).
Some researchers view the hippocampus as part of a larger medial temporal lobe memory system responsible for general declarative memory (memories that can be explicitly verbalized—these would include, for example, memory for facts in addition to episodic memory). Damage to the hippocampus does not affect some types of memory, such as the ability to learn new motor or cognitive skills (playing a musical instrument, or solving certain types of puzzles, for example). This fact suggests that such abilities depend on different types of memory (procedural memory) and different brain regions.
Finally we’ll discuss the hippocampus’ role in circadian rhythm, you know, that smooth Jazz band that your Uncle Larry listens to. No, the circadian rhythm is the cyclical output of hormone release. This timekeeping system, or biological “clock,” allows us to anticipate and prepare for the changes in the physical environment that are associated with day and night, energy needs of the body and brain, and sleep patterns thereby ensuring we will “do the right thing” at the right time of the day.
When I hear patients say things like, “I can’t fall asleep”, or “I fall asleep fine but then wake and can’t get back to sleep,” I think, “They have a screwed-up hippocampus” (or sometimes I think, “I’d really like a peanut butter sandwich” – but let’s not confuse things here).
Cutting through all my ridiculous attempts to bring my really stupid humor to a rather boring topic, let’s review some things about the hippocampus before moving on:
- It may be important in behavioral inhibition along with the prefrontal cortex
- It is very important in shunting working memory to long-term storage
- It is important in sorting and retrieving memories
- It may tie memories of special senses (smell) to events, people, or places
- It helps with hormone output as it connects to the hypothalamus and pituitary gland
- It may help tie emotional memories to the amygdala as we shall soon see
- And, it’s a fun word to say
Next we’ll discuss the amygdala. It sits at the end of the hippocampus, on both sides of the brain and I thinks it’s the name of a French, cream-filled pastry. Its central nucleus produces autonomic (non-conscious) components of emotion (e.g., changes in heart rate, blood pressure, and respiration) as well as conscious perception of emotion primarily through the prefrontal cortex (anterior cingulate cortex, orbitofrontal cortex, and dorsolateral prefrontal cortex). Important to note is that these pathways go both ways which controls emotional behavior, fears, and anxiety.
The amygdalae perform primary roles in the formation and storage of memories associated with emotional events. Research indicates that, during fear conditioning, sensory stimuli reach the amygdalae, particularly the lateral nuclei, where they form associations with memories of the stimuli, especially if there is a strong emotional connection. Memories of emotional experiences imprinted in reactions of synapses in the amygdala elicit fear behavior. Fear behavior may be described as what you’d experience if a grizzly bear tore your tent door off. Think of that for a bit and then I don’t need to describe the loss of digestive control, raw emotions surfacing, sweating, lump-in-stomach, loss of sexual desire, etc.
This technically happens through connections with a grouping of neurons in what’s called the central nucleus of the amygdalae and the bed nuclei of the stria terminalis (BNST). The central nuclei are involved in the genesis of many fear responses, including freezing (immobility), tachycardia (rapid heartbeat), increased respiration, and stress-hormone release. This is because it fires directly into the sympathetic nervous system (the flight, fight, or freeze system). So, stimulation of the amygdala causes intense emotion, such as aggression or fear.
An example of a strong stimulation of the amygdala would be a panic attack. Panic attacks are brief spontaneously recurrent episodes of terror that generate a sense of impending disaster without a clearly identifiable cause. PET scans have shown an increase in blood flow to the hippocampus, beginning with the right hippocampus (think right brain – more emotional) and then to the amygdala. Similar but attenuated blood flow increases occurs during anxiety attacks and prolonged stress.
Destructive lesions of the amygdala cause tameness in animals, and a placid calmness in humans characterized as a flatness of affect – no personality. Lesions of the amygdala can occur as a result of Urbach-Wiethe disease where calcium is deposited in the amygdala. If this disease occurs early in life then these patients with bilateral amygdalar lesions cannot discriminate emotion in facial expressions, but their ability to identify faces remains (the anatomical area for face recognition and memory is in the temporal cortex). This is a good example of how emotion in one area (amygdala) is linked with perception in another area (temporal lobe) to create an intense emotionally charged memory.
Any lesions of the amygdala or from the prefrontal cortex connections to the amygdala were shown to be primarily responsible for ‘flatness of affect’. This work eventually led to the psychosurgical technique of prefrontal lobotomies (my aunt had this done in the 1930’s and lived as a personality-less ‘vegetable’ for another 60 years). Remember the movie with Jack Nicholson, “One Flew over the Cuckoo’s Nest?” The prefrontal cortex sends inputs into the amygdala and severing this input obliterates the conscious connections to emotions, social behavior, and interaction leaving a flatness of affect directly proportional to the size of the lesion.
Likewise, the opposite is true with excitation – lack of inhibition, excessive motive, OCD-like behavior, excessively emotional, etc. Lesions may increase or decrease function of any particular area or its connections to or from such lobe. Remember, by ‘lesion’ we mean any interference, stimulation or abnormal function.
The amygdala combines many different somatosensory and visceral inputs—this is where you get your “gut reaction”. The link between prefrontal cortex (conscious awareness and decision-making), hypothalamus (hormonal response), and amygdala (emotional memory), likely gives us our gut feelings, those subjective yet protective feelings about what is good and what is bad.
One intriguing observation in ASD/Lyme Brain is the apparent enlargement of the amygdala. The concept of “allostatic overload” (McEwen 2004, and McEwen & Lasley, 2003) was coined hypothesizing a possible biological defect causing an overgrowth. The enlargement of the amygdala would explain an increased activity of amygdalar function in many individuals – a heightened level of fear and anxiety, chronic stress of an ‘overly sympathetic’ (by sympathetic I am referring to the sympathetic nervous system controlling fight or flight responses) state, and generalized avoidance of social situations.
The amygdala has dense neuronal connections to the visual centers, modulating many levels of visual stimulation. Such visual processing of faces is essential to brain development in the newborn. A child impaired with a lesion in amygdalar connections may fail to fire impulses and lay pathways to the right prefrontal cortex in particular, further leading to social behavior issues as the child ages.
The ventral (front) of the mesencephalon (Midbrain) makes dopamine, a neurotransmitter for the brain. This dopamine projects to a multitude of areas aiding many functions including the cortex for activation as well as the neostriatum. Think of the neostriatum as the “gateway” to the basal ganglia effecting both the direct pathway (which facilitates movement) as well as the indirect pathway (which defacilitates) movement. Long story short – losses in dopamine make the person slow and rigid, both muscular (as seen in Parkinson’s disease) and mental (as seen in the dementias).
The neostriatum is composed of three groups of neural structures: the putamen, the caudate and the nucleus accumbens. The putamen relays connections for movement of the peripheral. For instance, if you have lost dopamine to this area, you get the slow, rigid, masking, hypokinetic tremor in Parkinson’s disease. If you get too much dopamine to the putamen your arms will fling as in ballismus or chorea.
The caudate, instead of getting dopamine from the substantia nigra in the ventral mesencephalon, gets dopamine from the ventral tegmentum, AKA “mesolimbic area”. This area is turned-on by basic emotions. So, when dopamine from this area goes up, your caudate will fire and create motion not to the limbs like the putamen, but rather the face and muscles related to emotions, like eyebrows, lips, cheek muscles and so forth. This is why one cannot help but express facial expressions when experiencing emotions and trained experts, like police investigators, can tell if someone is telling the truth by reading their face. Your facial expressions go beyond volitional control.
The nucleus accumbens is the third portion of the neostriatum. It takes all “positive and euphoric” projections and tells the brain via direct pathway how awesome the experience was. In addiction, for instance, if someone takes one ‘hit’ of meth amphetamines, it will alter the amount of dopamine to the nucleus accumbens for the rest of their life. On a healthy note, the nucleus accumbens has an important role in pleasure including laughter, reward, and reinforcement learning, as well as fear, aggression, impulsivity, addiction, and the placebo effect. Yes, one can actually decide that they ‘like’ something and increase dopamine stores in the nucleus accumbens giving us some insight into optimistic personalities!
When someone has emotional, hyperkinetic disorders as in anxiety, insomnia, tics, OCD, ADHD or just poor behavior, the astute clinician should consider an autoimmune response to neostriatal tissue. Numerous research studies have proven that neostriatal antibodies, secondary to autoimmunity is second only to cerebellar antibodies in commonality. Continued firing of these limbic pathways creates neuronal highways, per say, and reinforces the problem.
It’s an interconnection, less like a subway map than the lines on a jigsaw puzzle. Yes, neuronal connections are more linear and defined, but what we’ll soon see is that neurons also communicate in ways we never dreamed of – through the glial cells that we once thought of as neural glue.
So what is a person to do????? Call our office – 651-739-1248